What Percentage Of Someone’S Genetic Background May Contribute To Alcohol Dependency?

Studies show that alcoholism is approximately 50% attributable to genetics.

Is there a genetic background for alcohol dependence?

How do genes influence alcohol use disorder? Alcohol use disorder (AUD) often seems to run in families, and we may hear about scientific studies of an “alcoholism gene.” Genetics certainly influence our likelihood of developing AUD, but the story isn’t so simple.

Research shows that genes are responsible for about half of the risk for AUD. Therefore, genes alone do not determine whether someone will develop AUD. Environmental factors, as well as gene and environment interactions account for the remainder of the risk. Multiple genes play a role in a person’s risk for developing AUD.

There are genes that increase a person’s risk, as well as those that may decrease that risk, directly or indirectly. For instance, some people of Asian descent carry a gene variant that alters their rate of alcohol metabolism, causing them to have symptoms like flushing, nausea, and rapid heartbeat when they drink.

1. Many people who experience these effects avoid alcohol, which helps protect them from developing AUD.** As we have learned more about the role genes play in our health, researchers have discovered that different factors can alter the expression of our genes.
2. This field is called epigenetics.
3. Scientists are learning more and more about how epigenetics can affect our risk for developing AUD.

Can our genes affect alcohol treatment? Scientists are also exploring how genes may influence the effectiveness of treatments for AUD. For instance, the drug naltrexone has been shown to help some, but not all, patients with AUD to reduce their drinking.

1. Research has shown that patients with AUD who also have variations in a specific gene respond positively to treatment with the drug, while those without the specific gene do not.
2. A fuller understanding of how genes influence treatment outcomes will help doctors prescribe the treatment that is most likely to help each patient.*** What is NIAAA doing to learn more? NIAAA has funded the Collaborative Studies on Genetics of Alcoholism (COGA) since 1989, with the goal of identifying the specific genes that influence alcohol use disorder.

In addition, NIAAA funds investigators’ research in this important field, and also has an in-house research emphasis on the interaction of genes and the environment. NIAAA is committed to learning more about how genes affect AUD so that treatment—and prevention efforts—can continue to be developed and improved.

How much of alcoholism is genetics?

Around 50% to 60% of a person’s risk for alcoholism is due to genetic factors. This means that genetics play a large role in alcoholism. But environmental factors and the interactions between genetics and the environment are also important.

What percentage of people who drink alcohol become dependent?

In contrast, about 1 in 30 adults is classified as alcohol dependent.

What is the candidate gene for alcoholism?

The only genes that have been consistently replicated to contribute to alcoholism susceptibility are polymorphisms in the alcohol-metabolizing enzymes: ADH and aldehyde dehydrogenase (ALDH). ADH oxidizes ethanol to acetal- dehyde.

Is there a genetic component to addiction?

Genetics: The Blueprint of Health and Disease – Why do some people become addicted while others don’t? Family studies that include identical twins, fraternal twins, adoptees, and siblings suggest that as much as half of a person’s risk of becoming addicted to nicotine, alcohol, or other drugs depends on his or her genetic makeup.

1. Finding the biological basis for this risk is an important avenue of research for scientists trying to solve the problem of drug addiction.
2. Genetics is the study of genes.
3. Genes are functional units of DNA that make up the human genome.
4. They provide the information that directs a body’s basic cellular activities.

Research on the human genome has shown that, on average, the DNA sequences of any two people are 99.9 percent the same. However, that 0.1 percent variation is profoundly important—it accounts for three million differences in the nearly three billion base pairs of DNA sequence! These differences contribute to visible variations, like height and hair color, and invisible traits, such as increased risk for or protection from certain diseases such as heart attack, stroke, diabetes, and addiction.

• Some diseases, such as sickle cell anemia or cystic fibrosis, are caused by a change, known as a mutation, in a single gene.
• Some mutations, like the BRCA 1 and 2 mutations that are linked to a much higher risk of breast and ovarian cancer, have become critical medical tools in evaluating a patient’s risk for serious diseases.

Medical researchers have had striking success at unraveling the genetics of these single-gene disorders, though finding treatments or cures has not been as simple. Most diseases, including addiction, are complex, and variations in many different genes contribute to a person’s overall level of risk or protection.

Is there a difference between genetic and Hereditary?

Difference Between Genetic and Hereditary Diseases –

• Genes are the materials present in our body which are responsible for transmitting traits from parents to offspring from one generation to another.
• Several spontaneous or induced gene mutations can result in defective or faulty genetic material, some of which will be acting as the basis for various types of inherited diseases, characteristically carrying these mutated changes from parents to offsprings.
• The main difference between these two terms lies in the fact that hereditary diseases have the potential of being carried from one generation to another whereas a genetic disease can either be hereditary or not, but there will always be a mutational change in the genome,

Is Type 1 alcoholism genetic?

Summary – Adoption studies investigating the relative contributions of genetic and environmental factors to a person’s susceptibility to alcoholism have identified two alcoholism subtypes that differ in their inheritance patterns as well as in other characteristics.

• A predisposition for type I alcoholism, which affects both men and women, requires the presence of a specific genetic background as well as certain environmental factors.
• This alcoholism subtype is characterized by mild or severe alcohol abuse, adult onset of the disease, a loss of control over drinking, and guilt and fear about alcohol dependence.

People with this alcoholism subtype generally exhibit high harm avoidance and low novelty-seeking personality traits and drink primarily to relieve anxiety. In contrast, type II alcoholism, which occurs more commonly in men than in women, primarily requires a genetic predisposition; environmental factors only play a minor role in its development.

Type II alcoholism is associated with an early onset (i.e., before age 25) of both alcohol abuse and criminal behavior and an inability to abstain from alcohol. The most common personality characteristic of type II alcoholics is high novelty seeking. These people consume alcohol primarily to induce euphoria.

The differences in heritable personality characteristics and the interaction of these characteristics with personal experiences (i.e., environmental factors) can explain the differences in inheritance mode, age of onset, symptoms, and course of type I and type II alcoholism.

These two alcoholism subtypes, however, represent only the prototypes or extremes of a continuous spectrum of manifestations of alcoholism. Many of the subtype characteristics (e.g., personality traits) are inherited independently of each other, and all possible combinations of personality traits occur ( Cloninger 1987 b, Svrakic et al.1993 ).

Thus, extensive variability exists in the individual’s predisposition for alcohol abuse and related behaviors ( Cloninger et al.1995 ). Nevertheless, high harm avoidance and high novelty seeking appear to be the traits most strongly predisposing to type I and type II alcoholism, respectively.

• The validity of this typology has been confirmed in numerous independent investigations, including studies of male and female twins in the United States ( Pickens et al.1991 ) and a replication of the original Stockholm adoption study.
• Although the replication study reproduced many of the findings of the original report, some discrepancies also existed.

The resolution of these discrepancies will likely require further studies in additional subject populations.

Is depression and alcoholism genetic?

Evidence of Co–Occurring Alcoholism and Depression in Animal Models – The potential link between depression and alcohol use also has been investigated in laboratory animals. Although depression in animals cannot be assessed the same way as in humans, some behavioral tests can be interpreted as representing counterparts of human depression.

Examples of these tests are the “Porsolt” or forced swim test, in which rats or mice are observed for the duration of their attempt to escape from a beaker of water, and the restrained stress test, a measure of the animals’ locomotor activity following a period of restraint in a plastic tube. In both of these tests, the animals exhibit greater activity when they are pretreated with antidepressant drugs.

Researchers have compared the results of behavioral tests for depression with voluntary alcohol consumption in defined strains of rodents. The results demonstrate variability in these animal models, similar to what is observed in human patients with depression and alcohol use disorders.

1. For example, a rat strain called Flinders sensitive rat (FSL), which is thought to be particularly vulnerable to behavioral depression, does not voluntarily consume alcohol (see table) (Overstreet et al.1992).
2. Conversely, Fawn–hooded rats (Rezvani et al.2002) and C57 mice (Elmer et al.1987), both of which also demonstrate behavioral depression, will drink alcohol.

Finally, P rats, which have been selectively bred for alcohol preference over many generations, do not respond to tests of behavioral depression (Godfrey et al.1997). Researchers also investigated the responses of these various animal strains to drugs that act on messenger chemicals implicated in alcohol’s effects on the brain.

1. These analyses found that animals that are sensitive to depression also are sensitive to drugs which are similar to the messenger chemical but show variable responses to drugs that affect the messenger chemical (for a review, see Rezvani et al.2002).
2. These findings lead to the conclusion that, as in humans, animal models for both alcohol intake and depression show variability and that the relationship between the two behaviors varies with the model used.

— John I. Nurnberger, Jr., Tatiana Foroud, Leah Flury, Eric T. Meyer, Ryan Wiegand References ELMER, G.I.; MEISCH, R.A.; and GEORGE, F.R. Mouse strain differences in operant self–administration of ethanol. Behavior Genetics 17(5):439–451, 1987. GODFREY, C.D.; FROEHLICH, J.C.; STEWART, R.B.; et al.

• Comparison of rats selectively bred for high and low ethanol intake in a forced–swim–test model of depression: Effects of desipramine.
• Physiology and Behavior 62:729–733, 1997.
• OVERSTREET, D.H.; REZVANI, A.H.; and JANOWSKY, D.S.
• Genetic animal models of depression and ethanol preference provide support for cholinergic and serotonergic involvement in depression and alcoholism.

Biological Psychiatry 31:919–936, 1992. REZVANI, A.H.; PARSIAN, A.; and OVERSTREET, D.H. The Fawn–hooded (FH/Wjd) rat: A genetic animal model of comorbid depression and alcoholism. Psychiatric Genetics 12(1):1–16, 2002.

Relationship Between Behavioral Depression, as Indicated by Behavior in the “Forced Swim” and “Stress–Open Field” Tests, and Voluntary Alcohol Consumption in Genetically Defined Rodent Strains

Strain	Forced Swim Test	Stress–Open Field Test	Voluntary Alcohol Consumption
Flinders sensitive rat	?	+	0
P rat	0	—	++
Fawn–hooded rat	?	+	+
C57 mouse	++	+	+

KEY: ? = response unknown + = sensitive to behavioral depression; voluntary alcohol consumption ++ = very sensitive to behavioral depression; high levels of voluntary alcohol consumption 0 = no sensitivity to behavioral depression; no voluntary alcohol consumption – = not tested The COGA project, conducted at several research centers across the United States, seeks to identify genes contributing to the development of alcoholism and related characteristics (i.e., phenotypes).

• This article describes some of the methods used by COGA investigators to define phenotypes related to the comorbidity of alcoholism and depression and summarizes data on both disorders in the COGA participants.
• Finally, the article discusses the implications of these findings for a potential genetic relationship between alcoholism and depression.

DESIGN AND METHODS OF THE COGA STUDY Between 1988 and 1998, investigators at six COGA sites used a common protocol to gather clinical information and biological data (including DNA and neurophysiologic measures) from families of subjects with alcoholism.

• Participants were recruited among patients undergoing alcoholism treatment (i.e., the probands) and their first–degree relatives.
• Control families were recruited from dental clinics, motor vehicle records, or random mailings at the six sites.
• Control families were not excluded if a family member had alcoholism or another psychiatric disorder; thus, these families represent a comparison group not selected with respect to psychopathology.

Each control family included at least two parents and three children ages 14 and older. All participants were interviewed using a screening instrument called the Semi–Structured Assessment for the Genetics of Alcoholism (SSAGA) (Bucholz et al.1994), which allows for diagnostic assessment of various disorders, including alcoholism and depression.

For the analyses presented here, participants were diagnosed with alcoholism (ALC) if they met the diagnostic criteria for alcohol dependence specified in the Diagnostic and Statistical Manual of Mental Disorders, Third Edition, Revised (DSM–III–R) (American Psychiatric Association 1987) as well as the criteria for “definite alcoholism” established by Feighner and colleagues (1972).

Participants were diagnosed with depression (DEP) if they met the DSM–III–R criteria for major depressive disorder or if they had “depressive syndrome.” (Subjects were classified as having depressive syndrome if they met all the criteria for major depressive disorder, except that the depression could have been caused by alcohol or other drug use or another illness.) Participants with both ALC and DEP were included in the phenotype “alcoholism and depression” (AAD).

People meeting the criteria for either ALC or DEP were combined into a phenotype called “alcoholism or depression” (AorD). Separate analyses were conducted for participants with the DEP phenotype—that is, with depression or depressive syndrome (which can occur in both alcoholics and nonalcoholics). The COGA researchers performed statistical analyses of differences in the prevalence of alcoholism and/or depression in various subgroups of study participants and tested interactions between variables.

These data were calculated for all families of alcoholic probands and for control families where appropriate. After the diagnostic assessment, a subset of families with at least two alcoholic members in addition to the initially recruited proband were invited to participate in a second stage of assessment, which included blood collection for genetic analyses.

For these analyses, the investigators checked a total of 336 short, repeated DNA sequences located throughout all chromosomes (for more information, see Reich et al.1998; Nurnberger et al.2001). These sequences are useful as markers because they vary in size from one person to another and their inheritance pattern can therefore be easily determined.

This screening process was carried out with two groups of participants. The first group (the “initial data set”) included 987 people from 105 families, and the second group (the “replication data set”) included 1,295 people from 157 families. To investigate the molecular genetics of alcoholism and depression, the COGA investigators performed linkage analyses.

This means that they compared the presence of certain variants (i.e., alleles) of the markers in people with the ALC, AAD, AorD, and DEP phenotypes to identify chromosomal regions that were more similar in people with a given phenotype than would be expected by chance. Such regions would be considered genetically “linked” to the phenotype—that is, they are located near a gene that influences the phenotype.

Because many genes appear to contribute to the risk for developing alcoholism, the investigators employed statistical methods that do not rely on specific models of susceptibility for the phenotype. All these statistical methods are based on the sharing of gene sequences that are identical by descent (IBD).

• Such sequences are considered IBD if both members of a sibling pair have inherited the sequence from the same parent.
• For further discussion of linkage analysis for complex disorders, see Nurnberger and Berrettini 1998.) The investigators conducted multipoint linkage analyses, in which multiple markers were evaluated simultaneously for evidence of allele (gene sequence) sharing using the computer program ASPEX ( ftp://lahmed.stanford.edu/pub/aspex/index.html ).

RESULTS OF THE COGA STUDY Prevalence of Alcoholism and/or Depression The COGA researchers first determined the prevalence of major depression and depressive syndrome in the families of the alcoholic probands (see table 2). These studies found that among both males and females, major depression was not more common in alcoholic participants than in nonalcoholic participants.

Table 2 Prevalence of DSM–III–R Depression and Depressive Syndrome in Adult COGA Probands and Their Alcoholic and Nonalcoholic Relatives

	COGA Probands and their Alcoholic Relatives	Nonalcoholic Relatives	Relative Risk Among COGA Probands and their Alcoholic Relatives
Males
Major Depression	11.0% (257/2,337)	10.5% (151/1,436)	1.05
Depressive Syndrome	30.3% a (707/2,337)	6.0% (86/1,436)	5.05
Total	41.2% a (964/2,337)	16.5% (237/1,436)	2.50
Females
Major Depression	24.2% b (311/1,288)	22.4% c (704/3,138)	1.08
Depressive Syndrome	32.8% a (423/1,288)	11.3% c (356/3,138)	2.90
Total	57.0% b (734/1,288)	33.8% c (1,060/3,138)	1.69

a X 2 ≥ 204 (actual values 315.4, 250.9, 290.9, 204.0, from top to bottom), df = 1, p < 10 –45 vs. nonalcoholic subjects. b X 2 ≥ 82 (actual values 108.6, 82.6), df = 1, p < 10 –18 vs. males. c X 2 ≥ 32 (actual values 92.1, 32.4, 144.7), df = 1, p < 10 –7 vs. males. NOTE: The data are from COGA Master File 86 (1999). The combination of alcohol dependence and depression (i.e., the AAD phenotype) appears to run in families, as demonstrated by an analysis of first–degree relatives of alcoholic probands with or without depression and first–degree relatives of control subjects. This analysis found that AAD occurred in 15.9 percent of first–degree relatives of probands with AAD (489 out of 3,069 people), compared with 11.7 percent of first–degree relatives of probands with alcoholism alone (287 out of 2,462) and 3.6 percent of first–degree relatives of control subjects (42 out of 1,164). Thus, the prevalence of AAD was significantly greater among the first–degree relatives of probands with AAD than among relatives of probands with alcoholism alone or relatives of control subjects (Nurnberger et al.2001). Next, the investigators determined the risks of alcoholism or depression for the relatives of three types of alcoholic probands—those with alcoholism alone, those with alcoholism and depressive syndrome, and those with alcoholism and major depression. The risk of alcoholism was significantly increased in the relatives of probands with both types of depression compared with probands with alcoholism alone (see table 3). Similarly, the risk of depression was increased in relatives of alcoholic probands with major depression and, to a lesser extent, in relatives of alcoholic probands with depressive syndrome. These findings support the idea that the AAD phenotype may represent a genetically distinct condition. This notion is further supported by the finding that depression in relatives of probands with AAD typically does not occur independently but only in combination with alcoholism. That is, the prevalence of major depression alone is not increased in those relatives. The prevalence of AAD, however, is increased twofold in relatives of probands with alcoholism plus depressive syndrome (i.e., 4.4 percent) and increased nearly fourfold in relatives of probands with alcoholism plus major depression (i.e., 8.4 percent) when compared with relatives of control subjects (i.e., 2.2 percent ). Another analysis (not shown on the table) found that the prevalence of depression alone is not significantly increased in relatives of probands with alcoholism alone (19.6 percent) or with the AAD phenotype (21.2 percent) compared with relatives of control subjects (19.3 percent). The prevalence of the AAD phenotype, however, is increased in relatives of probands with alcoholism only (10.2 percent) and in relatives of probands with AAD (14.3 percent) compared with relatives of control subjects (3.4 percent). These findings argue for a model in which some families carry susceptibility factors for both conditions. Finally, the increase in the prevalence of the AAD phenotype was seen in both male and female relatives of probands with alcoholism only or AAD.

Table 4 Prevalence of Alcoholism and Depression in the Relatives of Alcoholic and Control Probands in the COGA Study

	Diagnosis in Relatives
Proband Diagnosis	Alcoholism with or without Depressive Syndrome	Major Depression Only	Alcoholism and Major Depression
Control	10.2% (74/725)	14.6% (106/725)	2.2% (16/725)
Alcoholism with or without Depressive Syndrome	25.6% a (1,112/4,348)	13.1% (571/4,348)	4.4% a (191/4,348)
Alcoholism with Major Depression	24.0% a (132/549)	14.2% (78/549)	8.4%† (46/549)

p <,01 vs. control † p <,001 vs. alcoholism only and control NOTE: The data were derived from COGA Master File 86 (1999). The researchers also explored the order in which alcoholism or depression developed in both the probands and their relatives. For this purpose, the investigators determined the ages of onset of alcoholism and depression, which according to the DSM–III–R are defined as the ages at which three symptoms of alcoholism or the first major depressive episode, respectively, occurred. The analyses found that in approximately 50 percent of subjects with AAD, the onset of major depression occurred prior to the onset of alcohol dependence (see table 5). (For comparison, mania occurred first in about 42 percent of subjects with both mania and alcoholism.) This finding may indicate that even in this group of families with multiple cases of alcohol dependence, a substantial number of people develop alcoholism secondary to an underlying mood disorder. However, there was a notable gender effect in the order of disease onset: Males tend to develop alcohol dependence before the onset of the affective disorder, whereas this order tended to be reversed in females.

Table 5 Chronological Order of Disease Development in COGA Participants with Alcoholism and an Affective Disorder (i.e., Major Depression or Mania)

	Onset of Alcoholism First	Onset of Depression First	Same Time of Onset for Both Disorders
Alcoholism and Depression
Males (N = 267)	143 (53.6%)	104 (39.0%)	20 (7.5%)
Females (N = 325)	115 (35.4%)	193 (59.4%)	17 (5.2%)
Total (N = 592)	258 (43.6%)	297 (50.2%)	37 (6.3%)
Alcoholism and Mania
Males (N = 33)	22 (66.7%)	9 (23.7%)	2 (6.1%)
Females (N = 33)	13 (39.4%)	19 (57.6%)	1 (3.0%)
Total (N = 66)	35 (53.0%)	28 (42.4%)	3 (4.5%)

NOTE: The diagnoses and age of onset are based on data from COGA Master File 118 (2002). Linkage Analyses Because the data presented in the previous section suggested some interaction of vulnerability factors for alcoholism and depression, the COGA investigators performed genetic linkage analyses using DNA samples from sibling pairs with the AAD, AorD, and DEP phenotypes in order to identify chromosomal regions linked to these phenotypes.

In the sibling pairs, both siblings had the phenotype under investigation. This analysis included 224 AAD pairs (57 percent male), 1,359 AorD pairs (56 percent male), and 440 DEP pairs (49 percent male). The AorD phenotype is the most inclusive because it refers to people with either the ALC or DEP phenotypes.

Most of the sibling pairs added to the ALC data set to generate the AorD data set (59 percent of all added pairs and 94 percent of the mixed gender pairs) consisted of an alcoholic brother with a depressed sister. The results pointed to an area of interest on chromosome 1 for the AorD phenotype (Nurnberger et al.2001).

Increased allele sharing was seen near two markers called D1S1648 and D1S1588 between 100 and 110 centi–Morgan (cM) 1 from the origin. ( 1 A centi–Morgan is a unit of measurement for distances along chromosomes. The largest human chromosome, chromosome 1, has a length of approximately 325 centi–Morgan.

One can also express the location of markers as their distance in centi–Morgan from the tip of the chromosome.) This increased sharing was observed in the initial data set, to a lesser extent in the replication data set, and was still evident when the two data sets were combined.

Overall, the analyses found evidence for genetic linkage over a relatively large portion of chromosome 1 (i.e., 60 cM). (For a summary of other linkage results from these data sets, including results for the AAD and DEP phenotypes, see Nurnberger and colleagues 2001; see also the articles in this issue by Bierut and colleagues, pp.208–213 and by Edenberg, pp.214–218.) The same portion of chromosome 1 that exhibited linkage with the AorD phenotype also has shown suggestive linkage with the ALC phenotype (Reich et al.1998).

Analysis of all possible sibling pairs with the ALC phenotype in the initial data set identified a region near a marker called D1S1675. In sibling pairs with the ALC phenotype, allele sharing in that area was similar to the allele sharing observed in sibling pairs with the AorD phenotype.

1. In these families, the same genetic characteristics may predispose some people to depression and others to alcoholism.
2. IMPLICATIONS OF THE STUDY RESULTS The COGA study supports the conclusion of other investigators (Merikangas and Gelernter 1990; Merikangas et al.1994) that alcoholism and depression tend to occur together and that comorbid alcoholism tends to aggregate in the relatives of probands with both disorders.

The definition of depression in this analysis includes both major depression (i.e., primary depression) and depressive syndrome, which may be caused by alcohol and other drug use (i.e., secondary depression). However, primary and secondary depressive syndromes may not truly be distinct.

Many people with alcohol problems spend a substantial portion of their lives drinking and thus have less opportunity to demonstrate independent episodes of depression. An alcoholic with true vulnerability for depression may, by the natural course of the two illnesses, have no demonstrably independent episodes.

The genetic analyses demonstrated evidence for linkage of the AorD phenotype with a region on chromosome 1, and the same region also showed evidence, though less substantial, of linkage with the ALC phenotype. This chromosome 1 region also showed possible linkage with mania and depression among the participants in the NIMH Genetics Initiative Bipolar Study (Rice et al.1997).

Preliminary results suggested that this finding may be accounted for by families in which the probands have both alcoholism and mania. Thus, although the interpretation of linkage results in complex diseases is the subject of ongoing controversy and must be done cautiously, it appears likely that a locus on chromosome 1 accounts for some of the familial aggregation of alcoholism and depression in the COGA study.

The findings suggest that this region contains one or more genes associated with different clinical phenotypes (e.g., alcoholism, depression, and mania), a phenomenon called pleiotropy. The gene or genes associated with these phenotypes have not yet been identified.

• However, several genes that may influence central nervous system function have been mapped to that region on chromosome 1.
• For more information on genes located in that region, which is also referred to as the 1p13–35 region, see the Web site www.ncbi.nlm.nih.gov/locuslink,) Researchers await the results of other studies that may confirm these findings.

However, replication of linkage findings in complex disorders such as alcoholism and depression is likely to be difficult (Suarez et al.1994). In disorders to which multiple genetic factors contribute but for which no single factor is absolutely necessary, evidence for specific effects can differ among different data sets (i.e., for different study samples).

• Accordingly, the replication of any given effect may require several studies with data sets of a size equivalent to the original data set.
• The majority of participants with alcoholism in the COGA data set were male, and the majority of participants with depression were female.
• Of the sibling pairs added to the data set of alcoholic sibling pairs for the linkage analyses for the AorD phenotype, many consisted of a brother with alcoholism and a sister with depression.

Consequently, the gene or genes contributing to these vulnerabilities may have variable expression in men and women. This result is reminiscent of the concept of depressive spectrum disease as postulated by Winokur and colleagues (1971). The findings summarized in this article suggest a genetic relationship between depression and alcohol dependence in some families where both disorders are transmitted.

This conclusion is consistent with the idea that depression can be caused by many different genes (i.e., is a genetically heterogeneous condition). The results obtained so far have no direct implications for the treatment of patients with depression and/or alcohol dependence. However, they do reinforce the idea that some heavy drinkers may have genetic vulnerability to depression, as well as the observation that treatment of depressed alcoholic patients with antidepressants has generally had beneficial effects on the depression, and sometimes on the drinking as well (McGrath et al.2000).

In the future, genetic studies are likely to contribute to clinical treatment by identifying specific genes and their biochemical pathways, which could result in new therapeutic options for patient subgroups. The major advantage of the COGA study is its multisite design with similar methods employed at each site, which allowed the investigators to generate very large data sets.

• One limitation of the study is that by design it focused on families densely affected with alcohol dependence for linkage analysis (although all families of alcoholic probands are included in the prevalence studies).
• Although such families are ideal for genetic studies, they may not be fully representative of the spectrum of people who suffer from alcoholism, depression, or both.

Despite this limitation, the study’s results, in combination with prior studies, suggest that the pattern of disorders in the family is a reasonable clinical characteristic to use for the differentiation of subgroups within alcoholism. ACKNOWLEDGMENTS We acknowledge administrative support for the COGA project and these analyses from Henri Begleiter, M.D.; Ingrid Schmidt, at the State University of New York, Brooklyn; and Ting–Kai Li, M.D., at Indiana University.

• COGA involves nine different centers across the United States where data collection, analysis, and/or storage take place.
• The principal investigator of COGA is H.
• Begleiter, State University of New York, Health Science Center at Brooklyn.T.
• Reich, Washington University, is co–principal investigator.
• The study sites and their principal investigators and co–investigators are: Indiana University (T.K.

Li; J. Nurnberger, Jr.; P.M. Conneally; H. Edenberg); University of Iowa (R. Crowe, S. Kuperman); University of California at San Diego (M. Schuckit); University of Connecticut (V. Hesselbrock); State University of New York, Health Science Center at Brooklyn (B.

• Porjesz, H.
• Begleiter); Washington University in St. Louis (T.
• Reich, C.R.
• Cloninger, J. Rice, A.
• Goate); Howard University (R.
• Taylor); Rutgers University (J.
• Tischfield); and Southwest Foundation (L. Almasy).
• REFERENCES American Psychiatric Association (APA).
• Diagnostic and Statistical Manual of Mental Disorders, Third Edition, Revised.

Washington, DC: APA, 1987. BUCHOLZ, K.K.; CADORET, R.; CLONINGER, C.R.; et al. A new, semi–structured psychiatric interview for use in genetic linkage studies: A report on the reliability of the SSAGA. Journal of Studies on Alcohol 55(2):149–158, 1994. FEIGHNER, J.P.; ROBINS, E.; GUZE, S.B.; et al.

• Diagnostic criteria for use in psychiatric research.
• Archives of General Psychiatry 26:57–63, 1972.
• FOROUD, T.; EDENBERG, H.J.; GOATE, A.; et al.
• Alcoholism susceptibility loci: Confirmation studies in a replicate sample and further mapping.
• Alcoholism: Clinical and Experimental Research 24(7):933–945, 2000.

KENDLER, K.S.; HEATH, A.C.; and NEALE, M.C. Alcoholism and major depression in women. Archives of General Psychiatry 50:690–698, 1993. MCGRATH, P.J.; NUNES, E.V.; and QUITKIN, F.M. Current concepts in the treatment of depression in alcohol–dependent patients.

1. Psychiatric Clinics of North America 23(4):695–711, 2000.
2. MERIKANGAS, K., and GELERNTER, C.
3. Comorbidity for alcoholism and depression.
4. Psychiatric Clinics of North America 3:613–632, 1990.
5. MERIKANGAS, K.R.; RISCH, N.J.; and WEISMANN, M.M.
6. Comorbidity and co–transmission of alcoholism, anxiety, and depression.

Psychological Medicine 24:69–80, 1994. NURNBERGER, J.I., Jr., and BERRETTINI, W. Psychiatric Genetics, London: Chapman & Hall, 1998. NURNBERGER, J.I., Jr., and the NIMH Genetics Initiative Bipolar Group. “Evidence for a Locus on Chromosome 1 Influencing Alcoholism and Affective Disorders.” Paper presented at the World Congress of Biological Psychiatry, Berlin, July 2001.

NURNBERGER, J.I., JR.; FOROUD, T.; FLURY, L.; et al. Evidence for a locus on chromosome 1 that influences vulnerability to alcoholism and affective disorder. American Journal of Psychiatry 158(5):718–724, 2001. NURNBERGER, J.I., JR.; O’CONNOR, S.; MEYER, E.T.; et al. “A Family Study of Alcohol Dependence: Combining Sources of Diagnostic Information.” Paper presented at the International Genetic Epidemiology Society Meeting, New Orleans, November 2002.

REICH, T.; EDENBERG, H.J.; GOATE, A.; et al. Genome–wide search for genes affecting the risk for alcohol dependence. American Journal of Medical Genetics (Neuropsychiatric Genetics) 81:207–215, 1998. RICE, J.P.; GOATE, A.; WILLIAMS, J.T.; et al. Initial genome scan of the NIMH Genetics Initiative bipolar pedigrees: Chromosomes 1, 6, 8, 10 and 12.

1. American Journal of Medical Genetics (Neuropsychiatric Genetics) 74:247–253, 1997.
2. SCHLESSER, M.A.; WINOKUR, G.; and SHERMAN, B.M.
3. Genetic subtypes of unipolar primary depressive illness distinguished by hypothalmic pituitary adrenal axis activity.
4. Lancet 1:739–741, 1979.
5. SUAREZ, B.K.; HAMPE, C.L.; and VAN EERDEWEGH, P.

Problems of replicating linkage claims in psychiatry. In: Gershon, E.S., and Cloninger, C.R., eds. Genetic Approaches to Mental Disorders. Washington, DC: American Psychiatric Press, 1994. pp.23–46. WINOKUR, G.; CADORET, R.; DORZAB, J.; and BAKER, M. Depressive disease: A genetic study.

What percentage of men become alcoholics?

Men and Alcoholism – What Do the Statistics Tell Us? – According to all the data available on the topic of men and alcoholism, men are at a significantly greater risk to develop an alcohol addiction than women – by a lot. In fact, some estimates suggest that men are as much as four times more likely to be afflicted with alcoholism than women.

This is evidenced by a NIAAA report, which states that of the 88,000 people who die every year from alcohol-related death, an astounding 62,000 are men and only 26,000 are women. It is unclear why men are more likely to become alcoholic drinkers than women. However; one study suggests that the release of dopamine may be a huge factor.

This research revealed that men produce more dopamine (one of the brain’s “feel-good” neurotransmitters) while drinking, which reinforces continued drinking because it feels so good. It also showed that men are more likely to develop a tolerance to alcohol than women are, making them more likely to drink larger quantities of alcohol.

Approximately 58 percent of all adult men reportedly drank alcohol within the last month. Approximately 23 percent of men engage in binge-drinking at least five times per month, with an average of eight drinks per binge. Men are approximately two times more likely to binge drink than women. About 4.5 percent of all men meet the diagnostic criteria for alcohol dependence. Among all drivers involved in fatal motor-vehicle accidents, men are about twice as likely as women to have been intoxicated at the time of the accident. Men consistently have higher rates of alcohol-related hospitalizations than women. Men commit suicide more often than women (by about four times) and are much more likely to have been drinking alcohol when they committed suicide. Drinking alcohol increases the risk of cancer of the mouth, throat, esophagus, liver, and colon in men. An AUD can interfere with male hormone production and testicular function. This can result erectile dysfunction and infertility.

These statistics are sobering, to say the least. Because of social stigma, many men are not willing to admit they need help when their drinking gets out of hand. Cultural expectations can lead men to believe they are weak or “less of a man” if they admit defeat.

Who is at risk of alcohol dependence?

Risk factors – Alcohol use may begin in the teens, but alcohol use disorder occurs more frequently in the 20s and 30s, though it can start at any age. Risk factors for alcohol use disorder include:

Steady drinking over time. Drinking too much on a regular basis for an extended period or binge drinking on a regular basis can lead to alcohol-related problems or alcohol use disorder. Starting at an early age. People who begin drinking — especially binge drinking — at an early age are at a higher risk of alcohol use disorder. Family history. The risk of alcohol use disorder is higher for people who have a parent or other close relative who has problems with alcohol. This may be influenced by genetic factors. Depression and other mental health problems. It’s common for people with a mental health disorder such as anxiety, depression, schizophrenia or bipolar disorder to have problems with alcohol or other substances. History of trauma. People with a history of emotional trauma or other trauma are at increased risk of alcohol use disorder. Having bariatric surgery. Some research studies indicate that having bariatric surgery may increase the risk of developing alcohol use disorder or of relapsing after recovering from alcohol use disorder. Social and cultural factors. Having friends or a close partner who drinks regularly could increase your risk of alcohol use disorder. The glamorous way that drinking is sometimes portrayed in the media also may send the message that it’s OK to drink too much. For young people, the influence of parents, peers and other role models can impact risk.

Can you drink a lot and not be an alcoholic?

Press Release – Embargoed until: Thursday, November 20, 2014, Noon ET Contact: pdf icon 9 out of 10 excessive drinkers are not alcohol dependent 89.8%: Excessive Drinkers Who are Not Dependent 10.2%: Excessive Drinkers Who are Dependent Entire Infographic pdf icon Nine in 10 adults who drink too much alcohol are not alcoholics or alcohol dependent, according to a new study released by the Centers for Disease Control and Prevention in collaboration with the Substance Abuse and Mental Health Services Administration (SAMHSA).

• The study appears today in the CDC journal Preventing Chronic Disease,
• Excessive drinking includes binge drinking (four or more drinks on an occasion for women, five or more drinks on an occasion for men); consuming eight or more drinks a week for women or 15 or more drinks a week for men; or any alcohol use by pregnant women or those under the minimum legal drinking age of 21.

Alcohol dependence is a chronic medical condition that typically includes a current or past history of excessive drinking, a strong craving for alcohol, continued use despite repeated problems with drinking, and an inability to control alcohol consumption.

“This study shows that, contrary to popular opinion, most people who drink too much are not alcohol dependent or alcoholics,” said Robert Brewer, M.D., M.S.P.H., Alcohol Program Lead at CDC and one of the report’s authors. “It also emphasizes the importance of taking a comprehensive approach to reducing excessive drinking that includes evidence-based community strategies, screening and counseling in healthcare settings, and high-quality substance abuse treatment for those who need it.” The study found that nearly 1 in 3 adults is an excessive drinker, and most of them binge drink, usually on multiple occasions.

In contrast, about 1 in 30 adults is classified as alcohol dependent. The rates of alcohol dependence increase with the amount of alcohol consumed. About 10 percent of binge drinkers are alcohol dependent, while 30 percent of people who binge frequently (10 or more times a month) are alcohol dependent.

Excessive alcohol use is responsible for 88,000 deaths in the U.S. each year (including about 3,700 deaths from alcohol dependence), and cost the U.S. $223.5 billion in 2006. These deaths were due to health effects from drinking too much over time, such as breast cancer, liver disease, and heart disease; and health effects from drinking too much in a short period of time, such as violence, alcohol poisoning, and motor vehicle crashes.

Excessive drinkers who are dependent often need specialized or more intensive treatment to change their behavior. People who drink too much, but are not dependent, can still be encouraged to drink less through state and local interventions that increase the price and limit the availability of alcohol.

1. In addition those who are not dependent may be candidates for other clinical interventions, including screening and counseling offered by doctors and other health professionals.
2. CDC and SAMHSA scientists analyzed data on 138,100 U.S.
3. Adults aged 18 years and older from all 50 states and D.C.
4. Who participated in the National Survey on Drug Use and Health (NSDUH) in 2009, 2010, or 2011.

The survey includes a wide range of questions on substance use, including current drinking, binge drinking, average alcohol consumption, and symptoms of alcohol dependence. The Community Preventive Services Task Force recommends several evidence-based strategies to reduce excessive drinking, including increasing alcohol taxes, regulating alcohol outlet density, and holding alcohol retailers liable for harms resulting from illegal sales to minors or intoxicated patrons.

• The U.S. Preventive Services Task Force recommends screening and counseling for excessive drinking for all adult patients.
• This service is covered by most insurance plans, and can also be delivered by computer or telephone.
• For more information about excessive drinking, including binge drinking, and how to prevent this dangerous behavior, visit the CDC’s Alcohol and Public Health website at http://www.cdc.gov/alcohol/index.htm.

Members of the public who are concerned about their own or someone else’s drinking can call SAMHSA’s National Helpline at1-800-662-HELP to receive assistance from the Treatment Referral Routing Service. ### U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES external icon

What are the statistics of alcoholism?

Alcohol Use Disorder (AUD) in the United States: Age Groups and Demographic Characteristics People Ages 12 and Older According to the 2021 National Survey on Drug Use and Health (NSDUH), 29.5 million people ages 12 and older (10.6% in this age group) had AUD in the past year.1,2 This includes:

16.6 million males ages 12 and older (12.1% in this age group) 1,2 13.0 million females ages 12 and older (9.1% in this age group) 1,2 18.7 million White people ages 12 and older (11.0% in this age group) 1,2 3.5 million Black or African American people ages 12 and older (10.1% in this age group) 1,2 280,000 American Indian or Alaska Native people ages 12 and older (15.6% in this age group) 1,2 144,000 Native Hawaiian or other Pacific Islander people ages 12 and older (14.0% in this age group) 1,2 982,000 Asian people ages 12 and older (6.0% in this age group) 1,2 790,000 people of two or more races ages 12 and older (14.7% in this age group) 1,2 5.1 million Hispanic or Latino people ages 12 and older (10.3% in this age group) 1,2

Youth Ages 12 to 17 According to the 2021 NSDUH, 894,000 youth ages 12 to 17 (3.4% in this age group) had AUD in the past year.1,2 This includes:

298,000 boys ages 12 to 17 (2.2% in this age group) 1,2 596,000 girls ages 12 to 17 (4.7% in this age group) 1,2 526,000 White youth ages 12 to 17 (4.0% in age group) 1,2 48,000 Black or African American youth ages 12 to 17 (1.4% in this age group) 1,2 31,000 youth of two or more races ages 12 to 17 (3.4% in this age group) 1,2 235,000 Hispanic or Latino youth ages 12 to 17 (3.5% in this age group) 1,2 Estimates for American Indian or Alaska Native, Native Hawaiian or other Pacific Islander, and Asian youth ages 12 to 17 were not presented because they were based on a relatively small number of respondents or had a large margin of error.1,2

Adults Ages 18 and Older According to the 2021 NSDUH, 28.6 million adults ages 18 and older (11.3% in this age group) had AUD in the past year.1,2 This includes:

16.3 million men ages 18 and older (13.2% in this age group) 1,2 12.4 million women ages 18 and older (9.5% in this age group) 1,2 18.2 million White adults ages 18 and older (11.5% in this age group) 1,2 3.4 million Black or African American adults ages 18 and older (11.1% in this age group) 1,2 270,000 American Indian or Alaska Native adults ages 18 and older (16.7% in this age group) 1,2 118,000 Native Hawaiian or other Pacific Islander adults ages 18 and older (13.4% in this age group) 1,2 964,000 Asian adults ages 18 and older (6.4% in this age group) 1,2 759,000 adults of two or more races ages 18 and older (17.0% in this age group) 1,2 4.9 million Hispanic or Latino adults ages 18 and older (11.4% in this age group) 1,2

According to the Substance Abuse and Mental Health Services Administration (SAMHSA), caution should be used when comparing estimates from the 2020 and 2021 NSDUH to those from prior years due to methodological changes. Prior to the COVID-19 pandemic, data for NSDUH were collected during in-home visits, using computer-assisted techniques.

The COVID-19 pandemic necessitated a delay in data collection during 2020 and the introduction of web-based data collection, with very limited in-person data collection. The criteria used to categorize AUD among respondents also changed in 2020 from the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) to the fifth edition (DSM-5), resulting in some differences in whom is classified as having AUD.

Specifically, DSM-5 criteria could lead to a diagnosis of AUD for some respondents with too few symptoms to be diagnosed using DSM-IV criteria. Because these changes in data collection coincided with the spread of the COVID-19 pandemic and any related behavioral or mental health changes, we cannot fully separate the effects of methodological changes from true changes in the outcomes.

Can genetics play a role in alcohol tolerance?

Factors That Influence Alcohol Tolerance – Your alcohol tolerance is affected by your drinking habits, genetics, overall health and gender. No one person is the same when it comes to how much alcohol their system can handle. There are a lot of factors at play including:

• Genetics, gender and age
• Frequency and amount of drinking
• Your physical health
• Family history of alcohol abuse

If you feel like your tolerance for alcohol is getting out of control, it’s time to get help. Treatment options include counseling, therapy and support groups like Alcoholics Anonymous

What gene is missing for alcohol?

What causes alcohol intolerance? – A genetic metabolic disorder causes alcohol intolerance. When most people ingest alcohol, which contains ethanol:

• An enzyme called alcohol dehydrogenase (ADH) helps metabolize (process) the ethanol.
• Your liver converts the ethanol to acetaldehyde, a substance that can cause cell damage.
• Another enzyme called aldehyde dehydrogenase 2 (ALDH2) helps convert acetaldehyde to acetic acid (vinegar), which is nontoxic.

In people with alcohol intolerance, a genetic mutation (change) makes ALDH2 less active or inactive. As a result, your body can’t convert acetaldehyde to acetic acid. Acetaldehyde starts to build up in your blood and tissues, causing symptoms.

What gene is low alcohol tolerance?

Low Alcohol Tolerance Linked to Gene Researchers say they’ve identified a gene that makes some people more sensitive to the effects of alcohol, the reported Oct.19. University of North Carolina investigators conducted a genome analysis of 200 sibling pairs who had one parent with alcohol dependence but no alcohol problems themselves.

• Participants were then given the equivalent of three alcoholic drinks and asked to describe the effects.
• Their descriptions were compared with their genetic test results.
• The researchers found that participants with the gene CYP2E1 on chromosome 10 were less able to “hold their liquor” than participants without it.

The CYP2E1 gene is known to affect the way alcohol is metabolized in the brain. “Alcoholism is a very complex disease, and there are lots of complicated reasons why people drink. This may be just one of the reasons,” said Kirk Wilhelmsen, MD, PhD, lead author of the study.

Still, the researchers see the potential for developing a synthetic version of the gene to increase alcohol sensitivity — and thus decrease consumption — in the future. “Obviously we are a long way off having a treatment,” concluded Wilhelmsen. “But the gene we have found tells us a lot.” The study was published online Oct.19 in the journal,

: Low Alcohol Tolerance Linked to Gene

Are mental Health issues genetic?

Remember – Mental disorders are the result of both genetic and environmental factors. There is no single genetic switch that when flipped causes a mental disorder. Consequently, it is difficult for doctors to determine a person’s risk of inheriting a mental disorder or passing on the disorder to their children.

Can depression be passed down by genetics?

How common is major depression? At least 10% of people in the U.S. will experience major depressive disorder at some point in their lives. Two times as many women as men experience major depression. How do we know that genes play a role in causing depression? Scientists look at patterns of illness in families to estimate their “heritability,” or roughly what percentage of their cause is due to genes.

• To do this we find people with the disease who have a twin, and then find out whether the twin is also ill.
• Identical (monozygotic) twins share 100% of their genes, while non-identical (“fraternal” or dizygotic) twins share 50% of their genes.
• If genes are part of the cause, we expect a patient’s identical twin to have a much higher risk of disease than a patient’s non-identical twin.

That is the case for major depression. Heritability is probably 40-50%, and might be higher for severe depression. This could mean that in most cases of depression, around 50% of the cause is genetic, and around 50% is unrelated to genes (psychological or physical factors).

Or it could mean that in some cases, the tendency to become depressed is almost completely genetic, and in other cases it is not really genetic at all. We don’t know the answer yet. We can also look at adoption studies, to see whether an adopted person’s risk of depression is greater if a biological parent had depression.

This also seems to be the case. What about non-genetic factors? There are probably many non-genetic factors that increase risk of depression, many of which are probably not yet known. Severe childhood physical or sexual abuse, childhood emotional and physical neglect, and severe life stress are probably all risk factors.

• Losing a parent early in life probably also increases risk to some extent.
• If someone has a family history of depression, are they at very high risk? If someone has a parent or sibling with major depression, that person probably has a 2 or 3 times greater risk of developing depression compared with the average person (or around 20-30% instead of 10%).

The situation is a little different if the parent or sibling has had depression more than once (“recurrent depression”), and if the depression started relatively early in life (childhood, teens or twenties). This form of depression is less common – the exact percentage of the population is not known, but is probably around 3-5%.

1. But the siblings and children of people with this form of depression probably develop it at a rate that is 4 or 5 times greater than the average person.
2. Is there a “depression gene”? Some diseases are caused by a single defective gene.
3. Cystic fibrosis, several kinds of muscular dystrophy, and Huntington’s disease are examples.

These are usually rare diseases. But many common disorders like depression, diabetes and high blood pressure are also influenced by genes. In these disorders, there seem to be combinations of genetic changes that predispose some people to become ill. We don’t yet know how many genes are involved in depression, but it is very doubtful that any one gene causes depression in any large number of people.

• So no one simply “inherits” depression from their mother or father.
• Each person inherits a unique combination of genes from their mother and father, and certain combinations can predispose to a particular illness.
• How are major depression and bipolar disorder related? Most people who suffer from depression do not have episodes of mania.

We use the term major depression for depression without mania. Most people who experience mania also have major depression. We use the term bipolar disorder (or manic-depression) for this pattern. Major depressive disorder and bipolar disorder are the two “major mood disorders.” For more information on the symptoms of mania abd bipolar disorder, see the links at the bottom of this page.

1. Most people with major depression do not have close relatives with bipolar disorder, but the relatives of people with bipolar disorder are at increased risk of both major depression and bipolar disorder.
2. What about major depression and anxiety disorders? There are probably genetic changes that can increase the predisposition to both major depression and to certain anxiety disorders including generalized anxiety disorder, panic disorder and social phobia.

Also, some people have a more general lifelong tendency to experience unpleasant emotions and anxiety in response to stress. Psychologists use terms like “neuroticism” and “negative affectivity” to refer to this tendency, and people who have it are also more likely to experience major depression.

What is the meaning genetic predisposition?

Listen to pronunciation. (jeh-NEH-tik PREE-dih-spuh-ZIH-shun) An increased chance or likelihood of developing a particular disease based on the presence of one or more genetic variants and/or a family history suggestive of an increased risk of the disease.

Are genes from mom or dad?

How Do Genes Pass From Parent to Child? – To form a fetus, an egg from the mother and sperm from the father come together. The egg and sperm each have one half of a set of chromosomes. The egg and sperm together give the baby the full set of chromosomes. So, half the baby’s DNA comes from the mother and half comes from the father.

What genes are inherited from father only?

About Genetic Inheritance – You may be wondering, “what gene controls hair color ? ” or “what eye color will my baby have?” Most genetic traits result from a combination of both parents’ genetic codes. But when it comes to tracing certain traits to certain parents, we direct our focus to the genes contained in the sex chromosomes,

Through cell division and fertilization, humans acquire 46 chromosomes containing their unique DNA; 23 from mom, and 23 from dad. Sex-linked genes are expressed according to the genetic material on sex chromosomes, the 23rd pair, which differ between sexes. Where females have two X chromosomes, males have one X chromosome and one Y chromosome, with certain genetic traits found exclusively on either one.

Even still, some chromosomal genes are dominant or recessive, meaning that whether or not a characteristic is expressed depends on the alleles of mom and dad (respectively). If, for example, dad has an X-linked dominant gene, while mom has an X-linked recessive gene, the daughter’s outward gene expression will reflect dad’s genotype. Dads are responsible for the biological sex of their baby. I t’s one of the physical traits that’s 100% determined by paternal genes and/or dads. The Supporting Evidence : While mothers will always pass down their X chromosome (considering it’s the only kind they have), fathers will pass down either an X or Y chromosome at random.

The Y chromosome contains the SRY (male-determining) gene, which kickstarts the “virilization” (masculinization) process, including the fetal development of the testes—this means you have a baby boy on the way!

The X chromosome doesn’t contain this male-producing gene. Which means you’re having a baby girl!

The Big Picture : All of the physical differences between boys and girls are due to this tiny chromosomal difference. Dad’s contribution makes a big impact and can significantly affect the different genes your baby will carry! At least are responsible for determining height, coming from both mom and dad’s genes. But there is evidence to suggest that each parent’s “height gene” functions a bit differently. Dad’s genes play a significant role in promoting growth. The Supporting Evidence: The (IGF protein) is strongly expressed by paternal genes,

1. This genetic trait is also responsible for promoting growth.
2. However, mom’s genes express a somewhat contradictory receptor called IGF2R, which essentially does the opposite by actively repressing dad’s height-inducing genes.
3. These are both.
4. An imprinted gene is “stamped” or turned off, leaving the other gene to be expressed.

In this case, it doesn’t matter if Mom’s an Amazon when it comes to height or if Dad’s height is better suited for soccer rather than basketball – Dad’s IGF genes encourage the child to grow tall, while Mom’s IGF2R genes are stamped and rendered inactive.

• In essence, they cancel each other out.
• Illustrate this delicate balance between each parent’s genes and offspring development: Without expressing mom’s growth-suppressing IGF2R, the mice suffered from severe overgrowth.
• Without dad’s growth-promoting IGF protein, the mice experienced impeded growth and were smaller than average.

From an evolutionary standpoint., these genetic differences between mom and dad are called “,” which have an impact on growth and nutrition:

Paternal influence – Dad (more accurately, dad’s evolutionary adaptation) wants his son to grow big and strong in the womb. His genes use imprinting to give off signals during fetal development: “take nutrients from mom so you can be fit enough to survive life outside the womb.” Consuming more nutrients leads to increased growth, Maternal influence – Having a baby can certainly be an excessive nutritional demand on Mom-especially in the early ages of human evolution. To counteract this somewhat parasitic relationship, mom’s genes use imprinting to avoid the fetus needing so much sustenance, which can, in turn, suppress growth,

The Big Picture: Beyond the give-and-take of these two specific genetic expressions, there are loads more variants affecting height from both mom and dad. Dad’s genes strongly influence your child’s size in a certain sense, but whether your children grow up to be 6’5″ basketball stars or 5’10” point guards are up to certain genetic conditions from both parents. All men inherit a Y chromosome from their father, which means all traits that are only found on the Y chromosome come from dad, not mom. The Supporting Evidence : Y-linked traits follow a clear paternal lineage. A mutation on the Y chromosome can only be passed from father to son, and they’re all considered “dominant” in that there’s no second Y chromosome from mom to alter or mitigate the effects.

Hypertrichosis – Excessive hair growth on the outer ear Syndactyly – “Webbed toes,” where the skin between one or more toes is fused Chromosome infertility – Can affect the male’s sperm production

The Big Picture : For the most part, there’s no real indication that boys take after their dads in looks any more than they look like mom, but Y-linked traits are the exception to this rule. As we’ve learned, fathers contribute one Y or one X chromosome to their offspring. Girls get two X chromosomes, one from Mom and one from Dad. This means that your daughter will inherit X-linked genes from her father as well as her mother. When your daughter inevitably ends up with his X chromosome, does that mean she’ll inherit all of his X-linked genes and traits? Genes, yes.

• Traits, not necessarily.
• The Supporting Evidence : When it comes to a trait passed from father to daughter, dad has a 100% chance of passing down any mutations or variations on his X chromosome.
• However, this doesn’t automatically mean that all of these characteristics will present physically.
• While dad is passing down everything on his X chromosome, mom is also giving their daughter a second copy.

Only one copy of the allele (variation or mutation in a specific gene) is required for your daughter to develop the characteristic. If dad has the X-linked dominant gene, his daughter will undoubtedly present the trait because she inherits his X chromosome (where the gene responsible for the trait exists).

Fragile X syndrome Oral-facial-digital syndrome type I Incontinentia pigmenti type 1.

As for X-linked recessive : conditions, both parents’ chromosomal genes must contain two copies of the recessive trait in order to present physically. Dad’s genes are only half of the equation in this case. The Big Picture : While are a toss-up between mom and dad’s DNA, X-linked dominant features (when the allele variation is present in the father) is bound to make their way into your little girl’s life. There are a number of factors that go into the size and shape of our body, and genetics certainly has a lot to do with it. Dad’s adipose tissue, however, seems to have a bigger role in passing on excess fat compared to mom’s. The Supporting Evidence : Some body fat is necessary for general health and survival.

But, too much can lead to a number of health issues and complications. In the body, there are two types of fat cells that can be considered “good” or “bad.” Brown fat is responsible for burning calories and maintaining a safe body temperature. White fat, on the other hand, stores excess energy (calories) as fat.

have identified that brown fat is maternally inherited, while white fat is paternally inherited. This means that dad’s genes are more likely to contribute to the development of excess fat. Some health implications of obesity and excess fat include:

Heart Disease Diabetes High Blood Pressure Metabolic Syndrome

The Big Picture : Just because dad has a few extra pounds doesn’t mean your baby is destined for a similar fate. An active lifestyle and a healthy diet play a significant role for long-term health and wellness, regardless of parental genetics.

Do you inherit more DNA from mother or father?

Many of your relatives probably have an answer to the question of whether you are more your mother or your father’s child. But the correct answer to the question is not as simple as it might seem. Genetically, you actually carry more of your mother’s genes than your father’s.

• That’s because of little organelles that live within your cells, the mitochondria, which you only receive from your mother.
• Mitochondria are the energy-producing factories of the cell; without them, a cell would not be able to generate energy from food.
• Mitochondria have an interesting history, as about 1.5-billion to 2-billion years ago they were free-living organisms.

The ancestor of all mitochondria was a bacterium that was engulfed by another bacterium, but for one reason or another not digested, giving rise to the eukaryotes. The eukaryotes are basically all plants, animals and fungi, plus some rather weird organisms grouped together under Protista,

What is the heritability estimate for addiction to alcohol in both males and females?

It is considered that genetics contributes to alcoholism for about 50% for men and 25% for women (Reich 1998).

Which is a risk factor for alcohol use disorder?

Risk factors – Alcohol use may begin in the teens, but alcohol use disorder occurs more frequently in the 20s and 30s, though it can start at any age. Risk factors for alcohol use disorder include:

Steady drinking over time. Drinking too much on a regular basis for an extended period or binge drinking on a regular basis can lead to alcohol-related problems or alcohol use disorder. Starting at an early age. People who begin drinking — especially binge drinking — at an early age are at a higher risk of alcohol use disorder. Family history. The risk of alcohol use disorder is higher for people who have a parent or other close relative who has problems with alcohol. This may be influenced by genetic factors. Depression and other mental health problems. It’s common for people with a mental health disorder such as anxiety, depression, schizophrenia or bipolar disorder to have problems with alcohol or other substances. History of trauma. People with a history of emotional trauma or other trauma are at increased risk of alcohol use disorder. Having bariatric surgery. Some research studies indicate that having bariatric surgery may increase the risk of developing alcohol use disorder or of relapsing after recovering from alcohol use disorder. Social and cultural factors. Having friends or a close partner who drinks regularly could increase your risk of alcohol use disorder. The glamorous way that drinking is sometimes portrayed in the media also may send the message that it’s OK to drink too much. For young people, the influence of parents, peers and other role models can impact risk.

Is alcoholism a real disease?

Is addiction really a disease or a matter of choice? Ask the mother who lost her 19-year-old son — the laughing family prankster who earned a full-ride college scholarship as a solid student and star second baseman — to drugs. The moody, angry dropout who survived overdoses to get caught breaking into cars wasn’t the boy she raised.

What she knew, like the families and friends of the more than 15,000 Hoosiers who’ve died due to overdose since 1999, is that addiction’s not a life anyone would choose. Most medical professionals agree. The American Medical Association (AMA) classified alcoholism as a disease in 1956 and included addiction as a disease in 1987.

In 2011 the American Society of Addiction Medicine (ASAM) joined the AMA, defining addiction as a chronic brain disorder, not a behavior problem, or just the result of making bad choices. Research and input from top addiction authorities, addiction medicine doctors, neuroscientists and experts from the National Institute on Drug Abuse agree in classifying addiction as a disease.

What is ADH1B and ALDH2?

Background – The relationship between consumption of alcoholic drinks and stroke (including hemorrhagic and ischemic stroke) has been a long-standing debate, and results from previous epidemiological studies have been inconclusive, Alcohol may contribute to stroke by (1) inducing cardiac arrhythmias, which causes cardiogenic embolic stroke, (2) increasing the risk of hypertension in a linear positive dose-response manner in men and a J-shaped dose-response fashion in women,

In their meta-analysis to summarize the evidence from prospective studies on alcohol drinking and stroke types, Larsson et al. suggested that light and moderate alcohol consumption was inversely associated with ischemic stroke: in contrast, heavy drinking was associated with increased risk of all stroke with a stronger association for hemorrhagic strokes.

Alcohol metabolism is one of the biological determinants that can significantly influence drinking behavior and alcohol-related organ damage, Two key enzymes, alcohol dehydrogenase 1B (ADH1B) and aldehyde dehydrogenase 2 (ALDH2) are required to convert from alcohol to acetaldehyde and, eventually to acetic acid.

Genetic polymorphisms may increase the risk of alcohol addiction. Two single-nucleotide polymorphisms (SNP), rs1229984 (ADH1B), and rs671 (ALDH2), which are highly prevalent in Asians, have been shown to encode different versions of ADH and ALDH, The fast alcohol metabolizing ADH1B variant (ADH1B rs1229984 T or *2 allele vs.

C or *1 allele), and the inactive ALDH2 variant (ALDH2 rs671 A or *2 allele vs. G or *1 allele) cause rapid acetaldehyde accumulation and unpleasant alcohol flushing reaction; hence may inhibit alcohol consumption. The ADH1B T allele encodes a superactive enzyme subunit that has about 40 times faster maximum velocity than the enzyme encoded by the ADH1B C allele, and carriers of the ALDH2 inactive A allele has only about 0–17% of the residual activity as compared to the non-carriers,

• These two genetic variants are more prevalent among East Asians (~ 90% ADH1B T allele carriers and  ~ 40% ALH2 A allele carriers, respectively) than Caucasians (~ 10% ALDH1B T allele carriers and  ~ 0% ALDH2 A allele carriers, respectively),
• Even among different Asian ethnic groups, the prevalence of these two genetic polymorphisms varies.

For example, the ALDH2*2 allele appears to be most prevalent in Chinese–American, Han Chinese, and Taiwanese, Japanese, and Korean samples. Much lower rates have been reported among Thais, Filipinos, Indians, and Chinese and Taiwanese aborigines, Associations between stroke and these alcohol metabolism-related variants have not been widely reported in Asia.

A meta-analysis of 83 prospective studies with 5,99,912 current alcoholic beverage drinkers mainly of European descent suggested that stroke incidence increased steadily with the alcohol intake, This aligns with epidemiologic and genetic studies in China where U-shaped associations were found between self-reported alcohol intake and the incidence of ischemic stroke, intracerebral hemorrhage, and total stroke,

Moderate alcohol intake (100 g per week) was associated with a lower risk of stroke, However, genetic analyses showed no associations with ischemic stroke, intracerebral hemorrhage, or total stroke. We examined the relationship between genetic polymorphisms of ADH1B rs1229984, ALDH2 rs671, and stroke in relation to alcohol consumption among Taiwanese adults.