I recently read a scientific magazine which had done a research on genes and personality. It seems that our genes shape our personality in a range of 30 to 70%, no matter the conditions we were raised in and other environmental factors.
Whether we will become alcoholic, drug addicted, depressed, social, unfaithful, it is all written in our genes. And if it is written, there is a very big chance it is going to express itself.
Monozygotic twins - that is, twins born from the same "egg" and therefore share the same DNA - tend to develop similar personalities. Let's not forget that there are always twins born form two different "eggs" and hence do NOT share the same DNA.
Children that are adopted tend to develop personalities similar to their biological parents, instead of their foster ones.

Being curious, I did a small search on a gene found on chromosome 5. The gene is called HTR1A and is associated with depression and suicide.
Before you read, remember: This is only ONE gene. There are many others which I didn't bother to search, but I will name a few:

Gene FOXP2 ( Forkhead box 2) is foun on chromosome 7 and is associated with language and speaking development.


Gene AVR1A ( Vapopressin receptor) is found on chromosome 12 and is associated with loyalty and infidelity in erotic relationships.


Gene MAOB ( Monoamine oxidase B) is found on chromosome X and is associated with alcoholism and smoking.


Gene DRD4 ( Dopamine receptor D4) is found on chromosome 11 and is associated with extroversion and originality.


Gene HTR2C ( Serotonin receptor 2C) is found on chromosome X and is associated with compassion, mildness and friendliness.

And these are just a few.

Here's some of the things I found on HTR1A and depression:

Serotonin 5-HT1A, 5-HT1B, and 5-HT2A receptor mRNA expression in subjects with major depression, bipolar disorder, and schizophrenia.

Mental Health Research Institute, University of Michigan, 205 Zina Pitcher Place, Ann Arbor, MI 48109-0720, USA.

BACKGROUND: Alterations of serotonin neurotransmission are implicated in both mood disorders and schizophrenia. Specific serotonin-receptor-based abnormalities in these psychiatric illnesses have been intensively studied; however, it has been difficult to draw any conclusions because of a lack of consensus. These inconsistencies have most likely arisen from the unavailability of selective ligands.

METHODS: Our study used in situ hybridization to quantify 5-HT(1A), 5-HT(1B), and 5-HT(2A) mRNA levels in the hippocampus (HC) and 5-HT(1A) and 5-HT(2A) mRNA levels in the dorsolateral prefrontal cortex (DLPFC) of subjects with a history of major depression disorder (MDD), bipolar disorder (BPD), schizophrenia, and a normal comparison group (15 subjects per group).

RESULTS: In the DLPFC, there is a significant decrease in 5-HT(1A) mRNA of subjects with MDD and in 5-HT(2A) mRNA of subjects with BPD. Subjects with MDD have a significant decrease in 5-HT(1A) mRNA in the HC; subjects with BPD and schizophrenia had increased 5-HT(1B) mRNA levels and a significant decrease in 5-HT(2A) mRNA levels in the hippocampal formation.

CONCLUSIONS: Alterations in 5-HT(1A,) 5-HT(1B), and 5-HT(2A) mRNA levels in the brains of subjects with both mood disorders and schizophrenia add further support for hypothesis of dysregulation of the serotonergic system in these psychiatric disorders.


Attenuated 5-HT1A receptor signaling in brains of suicide victims: involvement of adenylyl cyclase, phosphatidylinositol 3-kinase, Akt and mitogen-activated protein kinase.

Department of Neuroscience, New York State Psychiatric Institute, New York, USA.

Positron emission tomography studies in major depression show reduced serotonin (5-HT)1A receptor antagonist-binding potentials in many brain regions including occipital cortex.

The functional meaning of this observation in terms of signal transduction is unknown. We used postmortem brain samples from depressed suicide victims to examine the downstream effectors of 5-HT1A receptor activation.

The diagnosis was established by means of psychological autopsy using Diagnostic and Statistical Manual of Mental Disorders (DSM) III-R criteria. Measurements of [35S]GTPgammaS binding to Galphai/o in the occipital cortex of suicide victims and matched controls revealed a blunted response in suicide subjects and a decrease in the coupling of 5-HT1A receptor to adenylyl cyclase.

No significant group differences were detected in the expression levels of Galphai/o, Galphaq/11 or Galphas proteins, or in the activity of cAMP-dependent protein kinase A.

Studies of a parallel transduction pathway downstream from 5-HT1A receptor activation demonstrated a decrease in the activity of phosphatidylinositol 3-kinase and its downstream effector Akt, as well as an increase in PTEN (phosphatase and tensin homolog deleted on chromosome 10), the phosphatase that hydrolyzes phosphatidylinositol 3,4,5-triphosphate.

Finally, the activation of extracellular signal-regulated kinases 1 and 2 was attenuated in suicide victims.

These data suggest that the alterations in agonist-stimulated 5-HT1A receptor activation in depressed suicide victims are also manifest downstream from the associated G protein, affecting the activity of second messengers in two 5-HT1A receptor transduction pathways that may have implications for cell survival.


And now comes the conclusion. Are we really NOT able to radically change ourselves if we wish so? Are we really not free to shape our personality in an entirely different way - for the better, hopefully - if we decide to do so?

We can't change our DNA. We can't change who we are "meant" to be. Are out genes some expression of the so called "fate"? And after all, is this even fair?