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Choline is a essential nutrient for humans it is consumed

in many foods.

It is a constituent of all cell membranes

and is necessary for growth and development. Also, as

the major precursor of betaine, it is used by the kidney

to maintain water balance and by the liver as a source of

methyl groups for the removal of homocysteine in methionine

formation. Finally, choline is used to produce the

important neurotransmitter (nerve messenger chemical)

acetylcholine, which is involved in memory and other

nervous system functions (Fig. 1). Maternal diets deficient

in choline during the second half of pregnancy in

rodents caused decreased neurogenesis and increased

neuronal apoptosis in fetal hippocampus (the memory

center), resulting in permanent behavioral (memory)

modifications in the offspring. Dietary deficiency of

choline in rodents causes development of liver cancer in

the absence of any known carcinogen. In humans, dietary

deficiency of choline is associated with fatty liver and liver


The dietary requirement for choline is influenced

by gender as well as by genetic polymorphisms.


Using a comprehensive database of the choline content of foods, a

number of epidemiological studies identified associations

between dietary choline intake and plasma homocysteine

levels (risk factor for cardiovascular disease), cancer, and

birth defects.



Choline is needed for synthesis of several major phospholipids

(phosphatidylcholine and sphingomyelin) in cell

membranes and is also involved in methyl metabolism,

cholinergic neurotransmission, transmembrane signaling,

and lipid–cholesterol transport and metabolism (1)

(Fig. 2). Choline can be acetylated, phosphorylated, oxidized,

or hydrolyzed. There are several comprehensive

reviews of the metabolism and functions of choline (1).

Cells absolutely require choline and die by apoptosis

when deprived of this nutrient (2,3). Humans derive

choline from foods, as well as from the de novo biosynthesis

of the choline moiety via the methylation of phosphatidylethanolamine

using (S)-adenosylmethionine as

the methyl donor (most active in the liver). This ability

to form choline means that some of the demand for

choline can, in part, be met by using methyl groups derived

from one carbon metabolism (via methyl-folate and

methionine). Several vitamins (folate, vitamin B12, vitamin

B6, and riboflavin) and the amino acid methionine interact

with choline in 1-carbon metabolism. There has been

renewed interest in these pathways during the past several

years, engendered by recent insights that indicate that

modest dietary inadequacies of the above-mentioned nutrients,

of a degree insufficient to cause classical deficiency

syndromes, can still contribute to important diseases

such as neural tube defects, cardiovascular disease, and

cancer (4).

Perturbing the metabolism of one of these pathways

results in compensatory changes in the others (1).

For example, methionine can be formed from homocysteine

using methyl groups from methyl-tetrahydrofolate

(THF), or using methyl groups from betaine that are

derived from choline. Similarly, methyl-THF can be

formed fromone-carbon units derived fromserine or from

the methyl groups of choline via dimethylglycine, and

choline can be synthesized de novo using methyl groups

derived from methionine [via (S)-adenosylmethionine].


Pathways of choline metabolism

Choline can be a methyl-group donor and interacts with methionine

and folate metabolism. It can be acetylated to form the neurotransmitter

acetylcholine, and it can be phosphorylated to form

membrane phospholipids such as phosphatidylcholine (lecithin)

and sphingomyelin. Choline can be formed via the methylation of

phosphatidylethanolamine (forming phosphatidylcholine, which

can be hydrolyzed to make choline).

use more methyl-THF to remethylate homocysteine in the

liver and increase dietary folate requirements. Conversely,

when they are deprived of folate, they use more methyl

groups from choline, increasing the dietary requirement

for choline (5). The availability of transgenic and knockout

mice has made possible additional studies that demonstrate

the interrelationship of these methyl sources (6).

When considering dietary requirements it is important to

realize that methionine, methyl-THF, and choline can be

fungible sources of methyl groups.

Choline is found in foods as free choline and as

esterified forms such as phosphocholine, glycerophosphocholine,

sphingomyelin, and phosphatidylcholine

(7). Lecithin is a term often used interchangeably

with phosphatidylcholine, whereas the compound is a

phosphatidylcholine-rich mixture added as an emulsifying

agent in the food industry. Pancreatic enzymes can liberate

choline from dietary phosphocholine, glycerophosphocholine,

and phosphatidylcholine. Before choline can

be absorbed in the gut, some is metabolized by bacteria

to form betaine and methylamines (which are not methyl


There is no estimate for percentage absorption of the

various forms of choline in humans. The water-soluble

choline-derived compounds (choline, phosphocholine,

and glycerophosphocholine) are absorbed via the portal

circulation, whereas the lipid-soluble compounds

(phosphatidylcholine and sphingomyelin) are absorbed

as chylomicrons. Lecithin is the most abundant choline containing

compound in the diet. About half of the lecithin

ingested enters the thoracic duct, and the remaining is metabolized

to glycerophosphocholine in the intestinal mucosa

and then to choline in the liver. The liver takes up

the majority of choline and stores it in the form of phosphatidylcholine

and sphingomyelin. The kidney and the

brain also accumulate choline. Although some free choline

is excreted with urine, most is oxidized in the kidney to

form betaine, which is responsible for maintaining the osmolarity

in the kidney. A specific carrier is needed for the

transport of free choline across the blood–brain barrier;

the capacity is especially high in neonates.


Choline and Epigenetics

Choline and other methyl donors are important dietary

modulators of epigenetic marks on genes. The term “epigenetics”

defines heritable changes in gene expression

that are not coded in the DNA sequence itself. Epigenetic

mechanisms include DNA methylation and histone modification.

DNA methylation occurs predominantly at the

cytosine bases followed by a guanosine (CpGs). When it

occurs in promoter regions that regulate DNA transcription,

the expression of the associated gene is altered (8,9).

Although there are exceptions, increased methylation is

usually associated with gene silencing, whereas decreased

methylation with induced gene expression. Another epigenetic

mechanism is histone modification (10). Histones

are proteins around which DNA is tightly wound, forming

the dynamic structure called chromatin. Chromatin can be

either an inactive state or an active state at which transcription

factors can pass through. Histone acetylation predominantly

promotes active chromatin, whereas histone

methylation can be associated with both transcriptionally

active and inactive chromatin. Furthermore, the degree of

methylation (mono-, di-, or tri-) results in distinct effects

on chromatin state (11). Methylation of DNA and histone

requires (S)-adenosylmethionine to methylate cytosines

in DNA and lysine and arginine residues in histones, respectively.

The availability of (S)-adenosylmethionine is

directly influenced by dietary choline and other methyl


Examples of epigenetic effects of choline and other

methyl donors include experiments in rodents in which

pregnant dams were fed diets that were choline deficient

versus normal, and DNA methylation in fetal brain was

modified, resulting in over expression of genes that inhibit

cell cycling in neural progenitor cells of developing brain

(12,13). Gestational choline availability also affects histone

methylation in the developing embryo, resulting in

changes in expression of genes that regulate methylation

and neuronal cell differentiation (14). Feeding pregnant

Pseudoagouti Avy/a mouse dams a choline and methylsupplemented

diet altered epigenetic regulation of agouti

expression in their offspring, as indicated by increased

agouti/black mottling of their coats and by lean body

phenotype (15,16). In another example, choline and

methyl donor supplementation to dams increased DNA

methylation of the fetal gene Axin fused [Axin(Fu)] and

reduced incidence of tail kinking in Axin(Fu)/+ offspring

by 50% (17). Thus, dietary manipulation of choline and

methyl donors (either deficiency or supplementation) can

have a profound impact upon gene expression.

138 Zeisel



In one of the first clinical nutrigenomics studies, humans

were phenotyped with respect to their susceptibility

to developing organ dysfunction when fed a low choline

diet (18–21). Adult men and women (pre- and

postmenopausal) aged 18 to 70 years were fed a standard

diet containing a known amount of choline (550 mg/

70 kg/day; baseline) for 10 days. On day 11 subjects were

placed on a diet containing less than 50 mg choline/day

for up to 42 days. Blood and urine were collected to measure

various experimental parameters of dietary choline

status, and markers of organ dysfunction and liver fat

were assessed. If at some point during the depletion period,

functional markers indicated organ dysfunction associated

with choline deficiency, subjects were switched

to a diet containing choline until replete.

Most men and postmenopausal women fed the low choline

diets developed reversible fatty liver (measure by

mass resonance spectroscopy) as well as liver and muscle

damage, whereas 56% of premenopausal women were

resistant to developing choline deficiency (21). The fatty

liver occurred due to lack of phosphatidylcholine synthesis

in liver, which is required for very low density lipoprotein

(VLDL) synthesis needed for export of excess triacylglycerol

from liver (22). Choline deficiency liver damage

was characterized by elevated serum aminotransferase

(23) and muscle damage was characterized by elevated

plasma serum creatine phosphokinase (19): both were due

to increased rates of apoptosis in these tissues (also occurred

in peripheral lymphocytes (24)). Choline-deficient

subjects also had impaired ability to handle a methionine

load, resulting in elevated plasma homocysteine concentrations


Only 44% of premenopausal women develop

signs of choline deficiency when deprived of dietary

choline as compared with most adult men and postmenopausal

women, suggesting their higher resistance

to choline deficiency (19,20). Premenopausal women required

less dietary choline because estrogen induces the

phosphatidylethanolamine-N-methyltransferase (PEMT)

gene to enhance the de novo biosynthesis of choline moiety

(26). Estrogen binds to its receptors, and this complex

interacts with estrogen response elements (EREs) in the

promoter of the PEMT gene, resulting in an upregulation

in PEMT mRNA expression and in hepatic enzyme activity

(26). Estrogen as the mediator of increasing PEMT activity

in women is important, especially during pregnancy

when fetal development uses a great deal of choline. Estradiol

concentration rises from 1 to 60 nMduring pregnancy

(27,28), suggesting that the capacity for endogenous synthesis

of choline should be highest when choline is needed

most. Pregnancy and lactation are stages of life that demand

high dietary choline intake and leave mothers extremely

vulnerable to choline deficiency (29). In utero,

the fetus is exposed to very high choline concentrations,

with a progressive decline in blood choline concentration

until adult levels of choline concentration are achieved

after the first weeks of life (30). Plasma or serum choline

concentrations are 6–7°ø higher in the fetus and newborn

than those in adults (31,32). High circulating choline in

the fetus and neonate ensures the availability of choline to


Less than 15% of pregnant women consume the recommended

adequate intake for choline (33), and in casecontrol

studies in California, women eating diets in the

lowest quartile for choline were at fourfold increased risk

for having a baby with a neural tube defect and at almost

twofold increased risk for having a baby with a cleft

palate; these risks were calculated after controlling for folate

intake (34,35).


Genetics of Choline Requirements

Although premenopausal women are more resistant to

choline deficiency, a significant portion of them (44%) still

develops organ dysfunction when deprived of choline,

suggesting individual differences in susceptibility to

choline deficiency. In fact, some men and women require

more than 850 mg/70 kg/day choline in their diet,

whereas others require less than 550 mg/kg/day (21).

Genetic variation likely underlies the differences in these

dietary requirements. A single-nucleotide polymorphism

(SNP) is a genetic variation occurring when a single nucleotide

(A, T, C, or G) in the genome sequence is altered.

These variations may affect metabolism. Only a few

reports investigate whether SNPs in the genes involved

in one carbon metabolism have roles in choline requirements

(36,37). Premenopausal women with a SNP in 5,10-

methylenetetrahydrofolate dehydrogenase (MTHFD1

rs2236225) were 15°ø more susceptible to choline deficiency

than did noncarriers. This variant increased the

use of choline perhaps by limiting the availability of

methyl-folate for Hcy remethylation and increasing the

demand for choline as a methyl-group donor. In addition,

individuals with a SNP in PEMT (rs12325817) were more

susceptible to choline deficiency, and women harboring

this SNP were more affected than did men. SNPs in

the PEMT gene alter endogenous synthesis of choline,

thereby increasing the dietary requirement for choline.

Dietary Recommendations

In 1998, the Institute of Medicine (IOM) made recommendations

for choline intake in the diet (4). At the time, there

were insufficient data with which to derive an estimated

average requirement for choline, thus only an adequate intake

(AI) could be estimated. The IOM report cautioned,

“this amount will be influenced by the availability of methionine

and methyl-folate in the diet. Itmaybe influenced

by gender, and it may be influenced by pregnancy, lactation,

and stage of development. Although AIs are set for

choline, it may be that the choline requirement can be met

by endogenous synthesis at some of these stages.”


Food Sources

In foods, there are multiple choline compounds that contribute

to total choline content (choline, glycerophosphocholine,

phosphocholine, phosphatidylcholine, and

sphingomyelin) (7). The U.S. Department of Agriculture

(USDA) maintains a database of choline content in

foods (38). Excellent sources of dietary choline are foods

that contain membranes, such as eggs and liver. Average

dietary choline intake on ad libitum diets for males and

females are 8.4 and 6.7 mg/kg choline per day.

Human milk is rich in choline. Choline is routinely added to

commercially available infant formulas. Until recently

some infant formulas had inadequate choline content (especially

soy-derived infant formulas), but in 2007–2008,

many infant formula companies increased the choline content

of their formulas so that they matched mature breast

milk. These formulas still have different mixtures of the

esters of choline than are present in human milk, perhaps

resulting in different bioavailability as compared to human

milk (41).

Adverse Effects

High doses of choline (>6 g) have been associated with excessive

cholinergic stimulation, such as vomiting, salivation,

sweating, and gastrointestinal effects (4). In addition,

fishy body odor results from the excretion of trimethylamine,

a choline metabolite from bacterial action (24). The

tolerable upper limit for choline has been set at 3 g/day (4).

Assessing Choline Status

Measurement of choline and choline metabolites is useful

in estimating choline status, but the measure is not definitive.

Plasma choline concentration varies in response to

diet and can rise as much as twofold after a two-egg

meal. Fasting plasma choline concentrations vary from7 to

15 M, with most subjects having concentrations of

10 M. Individuals that have starved for up to seven

days have diminished plasma choline, but levels never

drop below 50% of normal, probably because tissue phospholipids

are “cannibalized” to prevent concentrations

of choline from falling further (42). Note that children

during the first year of life have normal plasma choline

concentrations that are higher than 10 to 15 M (43).

Plasma phosphatidylcholine concentration also decreases

in choline deficiency (44), but these values are also influenced

by factors that change plasma lipoprotein levels.

Fasting plasma phosphatidylcholine concentrations

are approximately 1 to 1.5 mM. Thus, measurements of

choline or phosphatidylcholine in blood identify subjects

with low dietary choline intake, but provide little help in

differentiating the degree of deficiency.



Choline and betaine may benefit heart health by lowering

blood pressure, altering blood lipid profiling, and reducing

plasma Hcy, a risk factor for cardiovascular disease

(CVD) (45). Dietary choline intake was found to have a statistically

significant inverse relationship to circulating Hcy

concentrations in the Framingham Heart Study (46) and in

the Nurse’s Health Study (25), suggesting a protective effect

of choline intake. However, when looking at the association

between dietary choline intake and CVDincidence,

no association was found (14) in the European Prospective

Investigation into Cancer and Nutrition (EPIC) study

(47), and a marginal positive association was found in the

Atherosclerosis Risk in Communities (ARIC) study (48).

It is important to note that in the ARIC study, most individuals

in the cohort had choline intake below AI (49).

Hence, the effects of choline supplementation on CVD

risk remain unknown. Some human studies suggested

that high betaine supplementation increases plasma lowdensity

lipoprotein (LDL) cholesterol and triacylglycerol

concentrations (50–52), effects that might counterbalance

its Hcy lowering effects. However, the changes in serum

lipid concentrations were not associated with higher risk

of CVD. Moreover, the rise in LDL concentration may

be an artifact of increasing VLDL and triacylglycerol

excretion from fatty liver to plasma, which is not an adverse

outcome (for critical review see Ref. 53). The relationship

between choline and heart health warrants more


The choline-containing phospholipid phosphatidylcholine

has been used as a treatment to lower the

cholesterol concentrations because lecithin-cholesterol

acyltransferase has an important role in the removal of

cholesterol from tissue. Betaine, the oxidized product

of choline, has been used to normalize the plasma

homocysteine and methionine levels in patients with

homocystinuria, a genetic disease caused by 5,10-

methylenetetrahydrofolate reductase deficiency. Therefore,

dietary choline intake might be correlated with

cardiovascular disease risk. Many epidemiologic studies

have examined the relationship between dietary folic acid

and cancer or heart disease. It may be helpful to also consider

choline intake as a confounding factor because folate

and choline methyl donation can be interchangeable (7).



An interesting effect of dietary choline deficiency in rats

and mice has never been studied in humans. Dietary

deficiency of choline in rodents causes development of

hepatocarcinome in the absence of any known carcinogen

(54). Choline is the only single nutrient for which

this is true. It is interesting that choline-deficient rats not

only have a higher incidence of spontaneous hepatocarcinoma

but also are markedly sensitized to the effects of

administered carcinogens. Several mechanisms are suggested

for the cancer-promoting effect of a choline-free

diet. These include increased cell proliferation related to

regeneration after parenchymal cell death occurs in the

choline-deficient liver; hypomethylation of DNA (alters

expression of genes); reactive oxygen species leakage from

mitochondria with increased lipid peroxidation in liver;

activation of protein kinase C signaling due to accumulation

of diacylglycerol in liver; mutation of the fragile

histidine triad (FHIT) gene, which is a tumor suppressor

gene; and defective cell-suicide (apoptosis) mechanisms

140 Zeisel

(54). Loss of PEMT function may also contribute to malignant

transformation of hepatocytes (55).

Only a handful of epidemiologic studies explore

how choline and betaine intakes alter cancer risk in populations.

This was perhaps due to the absence of food composition

data, which has not been developed until recently

(7). The Long Island Breast Cancer Study found that high

choline consumption was associated with reduced breast

cancer risk (56), and high choline and betaine consumption

was associated with reduced breast cancer mortality

(57). Moreover, individuals with PEMT rs12325817 and

CHDH rs12676 SNPs had lower risk of developing breast

cancer, whereas BHMT rs3733890 had lower breast cancer

mortality. These data suggest the importance of nutrients

and genetic interactions in the etiology of cancer. Alternatively,

the Nurse’s Health Study II found no association

between choline intake and breast cancer risk (58), but a

positive association between choline intake and colorectal

cancer risk (59), suggesting different etiologies between

breast and colorectal cancer. More research is warranted.



Choline and Brain Development

In rodents, maternal dietary choline intake during late

pregnancy modulated mitosis and apoptosis in progenitor

(stem) cells of the fetal hippocampus and septum

and altered the differentiation of neurons in fetal hippocampus

(60). Variations in maternal dietary choline

intake (choline supplementation or choline deficiency)

during late pregnancy were also associated with significant

and irreversible changes in hippocampal function in

the adult animal, including altered long-term potentiation

(LTP) and altered memory (61). More choline (about 4°ø

dietary levels) during days 11–17 of gestation in the rodent

increased hippocampal progenitor cell proliferation,

decreased apoptosis in these cells, enhanced LTP in the

offspring when they were adult animals, and enhanced

visuospatial and auditory memory by as much as 30%

in the adult animals throughout their lifetimes (61). The

enhanced maze performance appears to be due to cholineinduced

improvements in memory capacity. Indeed, adult

rodents decrement in memory as they age, and offspring

exposed to extra choline in utero do not show this

“senility” (62). In contrast, mothers fed choline-deficient

diets during late pregnancy have offspring with diminished

progenitor cell proliferation and increased apoptosis

in fetal hippocampus, insensitivity to LTP when they

were adult animals, and decremented visuospatial and

auditory memory (61).

Early postnatal choline supplementation significantly

attenuated the effects of prenatal alcohol on a learning

task, suggesting that early dietary interventions may

also influence brain development (63). The mechanisms

for these developmental effects of choline are not yet clear.

Fetal alcohol syndrome (FAS) is an important concern of

pediatricians, with 1 in every 750 infants born with FAS

each year in the United States. Rats exposed to alcohol during

the perinatal period had poor performance on memory

tasks, which were improved by either prenatal or postnatal

choline supplementation (64,65). Rett syndrome (RTT),

a neurodevelopmental disorder associated with mutations

in the methyl-CpG-binding protein 2 (MeCP2) gene, is the

second leading cause of mental retardation in girls. RTT

girls experience a variety of deficits in cognitive, motor,

and social functions. In mouse models of RTT, enhancing

maternal or postnatal choline supplementation attenuates

motor coordination deficits and improves neuronal

integrity, proliferation, and survival (66,67). Choline supplementation

also ameliorates the symptoms in rodent

models of traumatic brain injury (68), status epilepticus

(69–71), and schizophrenia (72).

Are these findings in animals likely to be true in humans?

We do not know. Human and rat brains share many

elements of brain development but they mature at different

rates. In terms of hippocampal development, the embryonic

days 12–18 in the rat correspond to approximately

the last trimester in humans. Rat brain is comparatively

more mature at birth than is the human brain, but human

hippocampal development may continue for months or

years after birth.


Choline and Adult Brain

Acetylcholine is one of the most important neurotransmitters

used by neurons in the memory centers of brain

(hippocampus and septum). Choline accelerates the synthesis

and release of acetylcholine in nerve cells. Choline

used by brain neurons is largely derived from membrane

lecithin, or fromdietary intake of choline and lecithin. Free

choline is transported across the blood–brain barrier at a

rate that is proportional to serum choline level; lecithin

may be carried into neurons as part of an ApoE lipoprotein.

Choline derived from lecithin may be especially important

when extracellular choline is in short supply, as

might be expected to occur in advanced age because of

decreased brain choline uptake (73).

Results from studies using choline or phosphatidylcholine

to treat adults with brain disorders have been

very variable. Single doses of choline or lecithin in adult

humans may enhance memory performance in healthy

individuals, perhaps with greatest effect in individuals

with the poorest memory performance. Studies in students

showed that lecithin or choline treatment improved

memory transiently for hours after administration (74). In

humans with Alzheimer-type dementia, some studies report

enhanced memory performance after treatment with

lecithin (75), whereas other studies did not observe this.

Buchman et al. recently reported that humans on longterm

total parenteral nutrition may have verbal and visual

memory impairment, which may be improved with

choline supplementation (76). If lecithin is effective, it is in

a special subpopulation in the early stages of the disease.

Choline and lecithin have also been effectively used to

treat tardive dyskinesia, presumably working by increasing

cholinergic neurotransmission (77).



Choline in the diet is important for many reasons. Humans

deprived of it develop liver and muscle dysfunction, and

parenterally nourished patients need a source of choline.

As our understanding of the importance of folate and homocysteine

nutrition increases, there should be increased

interest in how choline interacts with these compounds.

Recent findings about choline in brain development in

animals should stimulate comparable studies in humans.

The availability of food composition data now makes it

possible to examine interactions between choline, folate,

and methionine when considering epidemiological data.


This work was supported by grants from the National

Institutes of Health (AG09525, DK55865). Support for this

work was also provided by grants from the NIH to the

UNC Clinical Nutrition Research Unit (DK56350).



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BiochemistrySuccess Chemistry Staff

Biochemistry describes and explores the molecular basis of living nature. Thematic and methodological overlaps exist with other disciplines, such as physiological chemistry, food chemistry, biotechnology, pharmacology, natural products chemistry or toxicology. For example, the collective field of molecular life sciences has established itself as the collective term for Molecular Life Sciences.

Biochemistry has made rapid progress in recent decades. More and more causes of disease and their molecular basis are understood. Methods and insights in biochemistry and molecular biology determine new developments in medicine, biotechnology, plant breeding & nutrition research. The structural understanding of biomolecules at the atomic level plays an increasingly important role.

Biochemists ask how living things or cells build or break down carbohydrates, fats, amino acids or hereditary molecules, and what amounts of energy are gained or consumed. They explore the structure and chemical composition of nucleic acids and the process of translating genetic information into physiological functions in a body cell.

They study how cell signaling works, which regulates the many metabolic pathways involved in breaking down and degrading, or how a fertilized egg can be used to create a complex organism with hundreds of different cell types. How does cancer develop? What causes death? How does our brain work? These are exciting questions whose answers biochemistry seeks on the molecular level.

Chemical knowledge and experimental competence play a key role here. Bioanalytics are refining modern separation and analysis methods, and technologies are increasingly penetrating into the single-molecule analysis. Tailored proteins are playing an increasingly important role in drug development alongside traditional substance libraries. Based on findings such as enzyme research, biochemists have the task of designing and synthesizing new biological agents with tailor-made properties.


Training in biochemistry

Is possible in several ways. In-Depth knowledge acquisition in biochemistry in the context of chemistry, biology or biotechnology studies can also be an alternative.

When taking up a bachelor's degree in chemistry with profiling in biochemistry, it is advisable to take additional biological basic lectures and internships as well as an introductory lecture in biochemistry. To specialize, you enroll in a bachelor's degree for a master's degree in biochemistry, attend biochemistry lectures and complete biochemical internships.

It is advisable, after detailed consultation, to additionally attend lectures and internships, especially in molecular biology, biophysical chemistry, and biophysics, genetics, cell biology, microbiology, biomedicine or related subjects. Solid knowledge in bioinformatics is also increasingly important. The required and offered study content and its scope vary from university to university.

At a number of universities, training as a molecular biologist or biochemist in biology studies is possible, with specialization in the master's program. Here conversely, in addition to lectures and courses in molecular biology and biochemistry, in particular knowledge in the branches of chemistry and biophysics should be made up and deepened.

An increasing number of universities offer their own biochemistry degree program. The program offers a cross-section between a chemical, biological, and some medical education and concludes - via the Bachelor - with the Master, mostly followed by a doctorate. An overview of the universities with the program Biochemistry is available in our university finder.

Some universities also offer additional special courses, in particular in the field of molecular biotechnology, molecular medicine, and medicinal chemistry. Despite medical references, these programs are usually affiliated with natural science faculties and lead to a master's degree, which is usually followed by a scientific doctorate.

In general, life sciences, with their strong interdisciplinary implications, are not always clearly defined in the curriculum. Anyone who has chosen this area as a career choice can also successfully enter biochemical research through training in organic chemistry, pharmacology, toxicology, pharmacy, physics or food chemistry. A suitable mix of appropriately trained professionals is increasingly being sought in the most strongly interdisciplinary research teams in science and industry. 


Biochemistry as a career

The career opportunities in the field of biochemistry are diverse. If you want to stay in basic research, you can find a job at universities and research institutes. Especially in the border area to medicine, there is an increasing need for research. Biochemists are increasingly in demand in the clinical area.

In the industry, there are companies in the pharmaceutical and biotech industries that have a need for biochemistry graduates for applications in "red" biotechnology. "White" biotechnology is also on the upswing, with which chemical companies produce plastics and everyday chemicals with environmentally friendly processes or from renewable raw materials, creating many new jobs.

As biocatalytic processes are increasingly used in industrial applications, protein biochemists are increasingly needed who have learned how to deal with enzymes, antibodies or other proteins. There are also interesting opportunities in the areas of crop protection, nutrition and in consumer-related sectors such as the food and cosmetics industry.

Interesting perspectives arise in addition to the production of active ingredients in product development and marketing. The area of public relations and administration in public authorities, associations and research institutes is also playing an increasingly important role. In addition, leadership positions in the chemical and pharmaceutical industries, as well as in management consultancy and finance companies are being filled by life scientists.