We Have to Hold Her Accountable… or How is She Going to Learn?

At the beginning of Risking Connectionâ training we discuss the differences between a traditional approach and a trauma informed approach. These include: The traditional approach maintains that the treater is the expert, and the client the recipient of this expertise; the main value in the traditional method is control and elimination of symptoms as opposed to collaboration and understanding the adaptive function of symptoms; and the idea that the treater should be unaffected by the work is replaced by understanding that all treaters are emotionally impacted by the work. 

As we finished this exercise in a recent training, one participant said: "I can see that in this method you do not hold the clients accountable. This will not work for me, I work in a juvenile justice facility and we have to hold the clients accountable or how will they ever learn?" Furthermore, she stated that she sees the clients as making choices, and her job to point out that there are consequences to these choices. 

This comment contains several of the most common fallacies or mis-beliefs about the trauma informed approach. We have to take these concerns seriously as they represent one of the largest obstacles to implementing this method. 

First of all there is the idea that we are recommending "not holding the client accountable". 

When you look up the definition of holding accountable you find it is associated with words like blame, find fault with, censure, to place the responsibility for, reproach, reprove, reprehend, criticize, to hold responsible; hold culpable. We don’t seem to speak of holding someone accountable for good things or positive achievements. 

We are as usual stuck in the middle of a dialectic- to use the words of DBT, the client is doing the best she can, and she needs to learn to do better. Our treatment must include both validation and a push for change. 

A child’s past and his current reality influence the choices he makes. If he is presented with the opportunity to steal a car and the urging of peers to do so, many things so influence whether he does or does not:

Does he have any self worth? Does he think there is any one who cares what he does? Has he learned values through loving attachments? Does he have a sense of hope for his life? Does he think he has anything to lose? Is he in the grip of intolerable anger, despair or fear and does he have any skills to manage whatever he is feeling? Is he mired in shame from other events and actions of his life? Does he have attachments with other friends or does he feel he will be alone forever if he alienates these friends? Does his mind have the capacity to think before he acts? 

If he decides to steal the car, gets caught, and is presented (involuntarily) to us for treatment, how can we best help him? What interventions on our part will result in him being more capable of turning away from him next opportunity to break the law? 

It would be neglectful to ignore the fact that he stole the car, to never mention it, or to act as though it was some how all right to have done so because of difficulties he has had in his past. 

It would also be neglectful to ignore the factors that contribute to his vulnerability to such actions. We would be less helpful if we did not offer treatment that increases his self worth, forms strong relationships, emphasizes the relationship consequences of behaviors, build up avenues for achievement and hope, helps him learn both emotion management skills and relationship skills, and teaches him how to calm his biology to increase his ability to think. 

A trauma informed approach confronts the behaviors directly. The treaters bring to the discussion respect, an assumption that every behavior is adaptive and solves a problem, information about change, a strong connection, and hope for a better future. 

In a trauma informed approach we answer the question: "how will he learn not to do this again?"

He will learn by a strong, respectful and straightforward investigation with his treaters of what happened and what contributed to his decisions.

He will learn through developing attached relationships. Within these he will learn values. He will have something to lose that matters. He will learn that he has strengths and talents. He will find hope. He will also learn through specific strategies to teach him emotion management and relationship skills. 

It’s not so much that we do not hold him accountable. It’s that caring and be cared about, skills and achievement offer so much more power for changes than simply explaining that if you steal cars you may go to jail. 

How would you answer this person’s comment? What are your views on this central concern about trauma informed care? We need to do much more thinking and talking about this. Click on “comment” and express your ideas.

 

 

 

 

 

 

 

 

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Beauty News: Anti-Ageing Perfume

Phtoto harveyprince.com If you care about the way you look and strive to look young - be careful how you smell! Rose is a no-no, grapefruit and apples are the right choice! Cosmeticsdesign-Europe.com reports that fragrance designer Harvey Prince has launched a new scent in the European market that makes other people perceive you as being much younger than you really are.This new anti-ageing

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ADHD Gene #7 SNAP 25 Gene

ADHD Genes

ADHD Gene #7: SNAP 25 Gene, T1065G allele, Human location: Chromosome #20 (20p11.2)

This will be our final installment in a series of 7 ADHD genes. Much of the information here is summarized in a publication by Faraone and Khan in a 2006 article in the Journal of Clinical Psychiatry. There will be further discussions on the topic of genes related to ADHD, so please stay tuned for future posts.

Nevertheless, the final ADHD gene, referred to in this post as SNAP 25, is of importance for discussion. SNAP 25 is short for the term "Synaptosomal-Associated Protein 25 Gene", which is located in the "p11.2" region on human chromosome #20. For more details on genes and gene locations and how they are relevant to our discussion on ADHD, please click here.

Of particular interest is the fact this SNAP25 gene is found to have a 100% match (meaning the DNA sequences are identical) in both chickens and mice. Because of this close match-up among the different species, genetic studies of this "ADHD gene" in mice (of which there are many) may provide information which is much more relevant to humans than other "ADHD genes" that have been covered. In other words, although the relative number of human studies involving this gene and ADHD is limited, a number of studies of the "mouse form" of this gene should be taken seriously.

In mice, a deletion (removal of part of a gene) for this gene results in spontaneous hyperactive behavior. Furthermore, motor abilities are noticeably compromised and physical changes to a part of the brain called the hippocampus (a part of the brain responsible for learning, memory development, emotional responses and various personality traits) were also seen. Therefore, some of the deficient "side effects" that are often seen in ADHD, such as poor memory, inappropriate emotional responses to certain situations and social maladjustments, may be affected, in part, by having the "ADHD form" of this gene. While the information surrounding this in humans should be viewed as only speculative at the present time, the direct behavioral correlations with the gene in mice are tough to ignore.

Unlike other ADHD genes, such as one in a previous post, where most of the "ADHD" behavior is tied to one single block of DNA, the correlation between the SNAP 25 gene and ADHD is more likely affected by multiple blocks of DNA on the gene. Nevertheless, the most statistically dominant form of the gene (also called allele, for more information on this, please click here) is thought to be what is called the T1065G allele. This "T1065G" notation means that the presence of a Thymine DNA base (Thymine is referred to as "T") instead of a Guanine ("G") at the DNA base 1065 (this a number is reference to where on the gene this replacement is located) results in a statistically-increased likelihood of developing ADHD.

If you are unfamiliar with the concept of DNA bases, please click here for a more detailed explanation.

While not of the statistical significance as the T1065G form, there is another nearby section of the gene that also may affect ADHD. In fact these two regions may "work together" to increase the likelihood of developing ADHD. This second form, which is backed by less statistical evidence than T1065G, is called the T1069C allele. This refers to a substitution of a Thymine (T) for a Cytosine (C) located on the 1069th base position in the gene. Keep in mind that these two regions are very close, separated by only 4 individual DNA bases. For more on what DNA bases are, please click here.

Among the key findings that we should draw from this research (as well as from other related studies) is this:
Individuals who have the "T" form at position 1065 in the gene instead of the "G" form are more likely to develop ADHD. Additionally, but to a lesser statistical degree, individuals who have the "T" form instead of the "C" at position 1069 are more likely to have ADHD as well. When combined (i.e. "T's" at both spots), the statistical likelihood of having ADHD goes up even further. Therefore, the SNAP 25 gene, located on the 20th chromosome in humans, is a good candidate gene to study and investigate for insight into an individuals genetic susceptibility to ADHD.

Again, if this explanation is difficult to visualize, please click here for another post with a relevant explanation.

Of course, SNAP25 is just one of many potential ADHD genes. However, if one is to have several of the "right forms" or alleles of multiple ADHD genes, the statistical likelihood of developing ADHD will continue to climb. Look for another post in the near future where I will summarize the results of the 7 "ADHD genes" that have been discussed in this section.

ADHD Genes

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ADHD gene #6. Serotonin receptor 1B gene (HTR1B)

ADHD Genes

ADHD Gene #6: Serotonin Receptor 1B (HTR1B), human chromosome #6 (section q13)

This is our sixth gene of topic in our discussion of ADHD genes. The Serotonin Receptor 1B gene (HTR1B). Like the 5 ADHD genes previously discussed, the gene HTR1B is thought to have at least some influence on the development of ADHD. (If you would like some more background information on what genes, chromosomes, DNA and alleles are, and how they relate to ADHD, please check out this link to another section of the blog here. I have outlined some of the specifics in this area). As its name suggests, this gene is responsible for creating a specific binding site (or think of a "docking site"), for the important neurochemical serotonin. Essentially, there are multiple forms of this gene, which is located on the 6th chromosome in humans (the "q13" refers to a more specific location of the gene on the chromosome, if you would like further explanation on how this looks, please click here).

As mentioned in another post, sometimes the smallest changes in DNA can produce noticeable results in the resulting biology, and ultimately, behaviors, of an individual. This gene appears to be no exception. At one specific point of this serotonin receptor gene (HTR1B), some individuals have a DNA base of "G" (short for "Guanine"), while others have the DNA base of "C" (short for "Cytosine", for more info on what this means, please click here). It appears that the simple change of one small piece of DNA from a "C" to a "G" on this particular "ADHD gene" can have a significant effect with regards to ADHD. Individuals with the "G" form of this particular gene are statistically more likely to have ADHD than those with the "C" form.

Furthermore, the connection with ADHD seems to be strongest to a particular subtype of ADHD. Individuals with the "G" form, or allele, tend to exhibit behavior that is more concentrated on what is referred to as the inattentive subtype of ADHD. The inattentive subtype, as its name suggests, is a form of ADHD in which the inability to maintain attention for a necessary period of time is the dominant negative attribute of the disorder (in contrast to other subtypes of ADHD, which have a more concentrated impulsive component, and/or hyperactive components, which are highlighted by highly impulsive or hyperactive behavior, respectively). While other genes may be tied to these other types of ADHD, the "G" form of the HTR1B serotonin receptor gene appears to be significantly correlated primarily with the inattentive ADHD subtype.

Please remember that the "G" form of this gene is not some weird mutation or genetic malfunction. It is a perfectly common form of the gene that is found in a number of regular individuals. Furthermore, there have been several studies done on this form or allele of the HTR1B gene, including one done on fraternal twins that did not show a significant correlation between the "G" form of the gene and the frequency of ADHD. Nevertheless, the data from several other studies, when pooled together, have strongly suggested a significant statistical correlation between the "G" form and the likelihood of exhibiting inattentive ADHD behavior. In other words, we should be cautiously optimistic about this association. Keep in mind, however, that the presence of this form of the gene, or any of the previously discussed "ADHD genes" does not, single-handedly, "doom" an individual to ADHD, it simply means that individuals with this form of the gene are statistically more likely to develop ADHD. We will be wrapping up this section of posts on ADHD genes with the seventh and final ADHD gene, the SNAP 25 gene, in tomorrow's blog.

ADHD genes

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Genetic terms and background information

ADHD Genes

Genes, Chromosomes, DNA and alleles: What are they and how do they relate to ADHD?

Author's Note: I realize that a lot of readers may not have any sort of background in genetics, which is why I constructed this page. If you are unfamiliar with how genes, DNA, Chromosomes, and alleles all tie together, this should serve as a great resource page. I tried to make it as straightforward as possible and use an analogy that makes the concept of genetics easy to follow. A number of other posts deal with the fact that a lot of causes of ADHD are inherited from parents to children. I am posting a number of sections on specific genes and alleles that are tied to the disorder of ADHD. Please check out the resources below:


Genes are comprised of long strings of DNA (typically numbering in the thousands or ten-thousands) and serve as a blueprint instructing the body as to:

1.) Which products (enzymes, hormones, etc.) to manufacture

2.) Where to manufacture the desired products

3.) How much of the products to manufacture

4.) When to stop, inhibit, or shut down manufactured products



Scientists generally agree that there are somewhere between 30,000 and 50,000 different genes in the human system.

DNA
DNA is short for the term Deoxyribo Nucleic Acid. It comes in four flavors or bases.

1.) Adenine (abbreviated as "A")
2.) Guanine (G)
3.) Thymine (T)
4.) Cytosine (C)

With all of the genetic diversity and variation among humans out there, it might seem strange that it all comes from four primary bases or options. However, we can see that, with four different options at every spot, we can build up a huge number of different possible sequences. Given the fact that the total length of DNA in humans is around 3 billion bases long, this means that there are an ENORMOUS number of possible combinations at our disposal.

For example, a segment of DNA may be in the following sequence: "CCGATA". This means that a Cytosine is strung to another Cytosine, which is connected to a Guanine, which is connected to an Adenine, which is connected to a Thymine, which is connected to another Adenine.

DNA's structure is typically in the helical form (think of a winding staircase). It can exist either in the single-stranded form or double-stranded form. The double-stranded form contains two strands bound together, winding up in staircase form called a double helix. The double-stranded form is relatively stable, because of a phemonomena called base pairing.

Base pairing:

The four DNA bases (A, T, C and G) tend to pair up with each other in what it called complementary base pairing. "A" tends to pair with "T" and "G" tends to pair with "C". In other words "A" and "T" are complementary, and "G" and "C" are complementary.

For example, consider our earlier sequence of "CCGATA": If this sequence is part of one DNA strand, the other one will typically match up with a complementary strand of "GGCTAT".

Do you see how that works?
CCGATA <---- strand 1 GGCTAT <---- strand 2
The C's on strand 1 match up with the G's on strand 2, the A's on strand 1, match up with the T's on strand 2 and vice versa. This pairing up and bonding between the two strands of DNA makes the DNA double helix quite stable. Since we know how the strands match up with each other, if we can find out the sequence of one strand, we can figure out what the other one would look like. For example, if we have one strand that has the following sequence:

AAATTGCCG

we can predict that the other one will "match up" with

TTTAACGGC.

Again, the A's from one strand match up with the T's from the other and the G's from one strand match up with C's from the other and vice versa.


Genes and DNA: The "highway and towns" analogy

Genes actually make up a relatively small percentage of the body's total DNA (thought to be less than 10 or 15%). One of the best ways to think of this is to envision a large highway that connects a number of towns together, but also passes along through long stretches of open country. The "highway" is the DNA, while the towns, (where the functional stuff "happens") are analogous to the specific genes. The stretches of highway in between the towns serve a limited function; their main purpose is to serve as a buffer space between the important towns. Similarly, the vast majority (over 85%) of DNA is not in the genetic region and is of limited function.

Since there are so many genes (towns), in humans, it would make more sense to create multiple highways to incorporate all of them instead of having just one long one. Essentially this is what nature does. It subdivides the DNA into different “bundles” or "groups" called chromosomes. The number of different “highways” varies from species to species; in fruit flies, the number of highways is 4, in humans, the number is 23. Additionally, human beings actually have two “pairs” of highways, one coming from each parent. Going back to our road analogy, think of our highway as a divided one, with one way going eastward and the other going westward. The two highways are “paired up”, that is, they go through the same towns and cover the same stretches of land in between, but there are now two highways instead of one. Therefore, with humans, we (typically) have 23 pairs of chromosomes (highways), for 46 total.

For humans, one of those pairs of highways is sex-determinant. If both highways are marked “X”, then you are female, if one of your highways is “X”, but the other is “Y”, then you are a male (you cannot have both highways or chromosomes as “Y” because your mother can only pass on an “X” chromosome, while your father can pass on either an “X” or a “Y”). While sex determination is a critical function of the sex chromosomes, it is important to realize that these “X” and “Y” highways also contain a number of genes themselves. These genes are referred to as “sex-linked”. If certain traits or inherited disorders show up exclusively or highly disproportionately in males or in females, chances are, at least one “sex-linked” gene is responsible.

Doing a bit of math we can see that with around 30,000-50,000 different genes (towns) and 23 pairs of chromosomes (highways), we would expect a typical highway to contain somewhere from 1000 to 2000 genes (towns). While the number of genes are not evenly distributed (some chromosomes or highways are larger than others), 1000-2000 genes per chromosome is a good estimate. Keep in mind, too, that the genes or towns vary in size as well; some may be cover a much longer stretch of highway than others. The distribution of genes among chromosomes normally does not vary from individual to individual, so you, your sister, your best friend and your next door neighbor will all typically have the exact same number of genes in the exact same order on a particular chromosome.

Taking this analogy a bit further, where we can identify a certain town as a "gene", we can further subdivide that town into smaller sections (think of individual blocks within a town). For example, one of the “ADHD genes” called the Dopamine Beta Hydroxylase Gene (DBH), has a location of “9q34”. What that means is that this gene is located on Chromosome #9 (“Highway 9” to follow the analogy), section “q34”. “q34” actually does not refer to one particular town, it still covers a slightly larger space than that (think along the lines of a county), but it does help narrow the location down quite a bit. Further numbers or letters beyond the “34” (which typically follow a “.”, such as “34.1”), can help narrow the location down even further to the city, and eventually block or even specific building level.

Alleles:
As mentioned, almost all humans carry the same number of genes in the same order, on the same chromosome. In other words, town #487 on chromosome 12 will be the same “gene” for you, as it is for Bob. Additionally, most of the blocks in your 487th town will look exactly the same as they would in Bob’s 487th town. However, there are some specific blocks that will show some variation between your town and Bob’s town. These slightly different forms of the same town are what are referred to as alleles (slightly different forms of the same gene).

Some genes have different alleles that differ in only one spot. For example, the first 8 blocks of your town and Bob’s town may contain the exact same buildings in the same order, but the 9th block in Bob’s town may contain a McDonald’s while yours contains a Burger King. Also, some alleles may differ by having a slightly longer or shorter segment for a particular block. For example, Bob’s town (allele) may have an extra gas station between blocks 15 and 16, while yours may have additional park space between blocks 19 and 20. A genetic analogy to this would be having a few extra pieces of DNA than Bob in a particular section of a gene.

Either way, it is important to remember that your genes and Bob’s genes are over 99% identical, there are just some minor differences such as those mentioned above. However, even these minor differences can have a number of prolific effects. For example, if your town and Bob’s town have the same number of residents, but Bob’s has 3 more gas stations than does yours, who do you think will be better adapted to supply enough gasoline for the town in the event of a fuel delivery truck failing to show up on a particular day? If your town has one additional power station than Bob’s, and a recent heat wave pushes up the power demand for a week, whose town will be better suited?

Similarly, a few small differences in individual variations of the same genes can play notable roles when dealing with disorders such as ADHD. A few key changes can significantly enhance or inhibit levels key proteins or neural chemicals. For example, the compound dopamine is an important signaling agent in the nervous system in which adequate levels are needed for proper brain function in areas such as maintaining an attention span. Not surprisingly, a number of ADHD individuals have lower than normal levels of dopamine in the frontal regions of the brain. Certain genes are responsible for producing key enzymes that aid in the manufacture and delivery of this important brain-friendly compound. Unfortunately, some forms or alleles of these genes are less effective in manufacturing these key enzymes. As a result, individuals with these alleles are more prone to dopamine imbalances in key regions of the brain. As a result, they are more prone to having ADHD. In the context of attention deficit disorders (ADD) and attention deficit hyperactivity disorders (ADHD), we will examine which forms or alleles of specific genes are tied to ADHD.

ADHD Genes

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Beauty Buzz: New Makeup Autumn 2008

Yves Saint LaurentThe YSL look for Autumn/Winter 2008 was inspired by "one of Yves Saint Laurents famous designs - the tuxedo". Well, I was not very inspired by the collection.Here is YSL new collectionPalette Collection for Face- POUDRE COLLECTOR POUR LES YEUX (limited edition)Collector Powder For The Complexion - POUDRE COLLECTOR POUR LE TEINT (limited edition)DESSIN DES LÈVRES - Lip Liner (8

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Beauty Buzz: New Makeup Autumn 2008 Part 4

ShiseidoShiseido's look for Autumn/Holliday season is Intriguing Elegance.The new products include: 2 new pallettes of Silky Eye Shadow Quad in Rose Tones and Wood Tones 5 new colors of Automatic Lip Crayon Accentuating Color Stick 2 new colors of Lip GlossPhotos from: Shiseido.com See other posts for:- Chanel New Makeup Autumn 2008 - Lancome Autumn 2008 Collection- Guerlain Makeup Collection

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The Role of the Clinician and of Formulation

Trauma informed care depends on clinical thinking. What is clinical thinking? It is looking beneath the behavior of the moment, and asking why? What’s going on? It is understanding that symptoms are adaptations that behavior has reasons, that people are doing the best they can, and that their behavior is solving a problem for them. The job of the clinicians in a treatment program is to be the standard bearers for clinical thinking, to teach and train the team until this sort of inquiry is second nature to all members of the team.

So when a child care worker reports that Monique ran away last night, and wants to know what her consequence should be, the clinician should divert the discussion to the question of “why”. What was going on last night? What was the provoking incident? What is going on in Monique’s life? What are her sources of stress, her worries, her fears? What are her strengths, what good things are happening for her that could be brought into the equation? What internal and external resources does she have?

In a congregate care treatment program there is considerable pressure for a clinician to turn away from clinical thinking and become a “fixer”. Some times it seems that clinicians’ job is to take away a screaming child and bring her back calm. The clinician may be drawn into thinking that what she is supposed to do with the child is talk to him about what he has done wrong and how if he stopped doing it his life would be much better.

The problem with this approach is that it doesn’t work. If it did, the kids would be much better already because this has been done a thousand times before. The job of the clinician is first of all to form a healing relationship with the child, then to use this relationship to help the child learn their own worth, develop connections that can be accessed even when the clinician is not present, and learn emotion management skills.

The clinician should have a complex and ever increasing understanding of the child, what their experiences have been, and how those experiences have shaped them. The clinician should hold in his mind a clear picture of the healed child- of who this child can become. He holds the hope for the child, even when the child can see no hope.

Similarly, in family therapy the clinician can get trapped into endless discussions of behavior and consequences. Instead, she must understand and honor the rich complexities of the family’s life. What is their history, their trauma, their pain, their strengths? What are the dynamics between family members, including extended family? What are their resources? What are their fears, what paralyzes them? The healing relationship, connection, developing self-worth and emotion management skills are equally important with the family.

Clinicians should be taught the art of formulating a case. A formulation makes explicit the clinician’s best understanding of the child’s history, their current circumstances, the effects these have on the child, how we understand their current behavior in light of their situation, and what we think will be the path for growth and change necessary to develop healthier methods for meeting needs.

The formulation should be one to two paragraphs which provide a clear road map for understanding and for treatment. Of course it is ever changing and evolving as we come to understand the child and family better.

In one program I heard described (Germaine Lawrence in Boston, http://www.germainelawrence.org/) they have a practice that every time they talk about a child, they start with a quick repetition of the formulation by the clinician, just to remind them of their road map and where they are on it. I thought this was a great idea.

Here are some examples of formulations:

1. Sarah suffered early neglect and abuse followed by repeated moves. Her siblings were adopted but she failed the placement. She struggles to maintain safety by keeping her fears hidden in oppositionality. She sees danger every where and over reacts with physical and verbal aggression. Her processing difficulties contribute to this misapprehension of events. She responds to care givers with suspicion but does react to limits. She will need to develop safety and trust in order to be able to relax, to explore her past and decrease her conviction that what has happened to her is her fault.

2. Thomas is a young man whose genetic heritage suggests that he might be vulnerable to a mood disorder. Multiple stressors have apparently exacerbated this biological predisposition. These stressors have included inconsistent parenting, being a witness to domestic violence, physical and emotional abuse, emotional, medical and educational neglect, and the death of his mother. Thomas’ most likely felt overwhelmed by these stressors and developed a negative coping style that resulted in his trying to “shut down” or avoid painful thoughts and experiences. When he was forced to be reminded of these painful experiences and when he had to incur more stress during times when adults were not able to limit his exposure to it, Thomas would rapidly become disorganized and resort to primitive defenses as evidenced by his becoming aggressive, suicidal, and even by his reporting psychotic symptoms.

Based upon reports of his progress in previous programs, Thomas seems to be able to utilize the structure of residential treatment to afford him the predictability and safety he needs in order to organize his thoughts and demonstrate his desire to behave in a socially acceptable way. His treatment goals should focus on increasing his ability to identify and practice positive coping skills to manage overwhelming affect, and on developing age-appropriate social skills.

3. Vanessa had early experiences with severe neglect and observing domestic violence because of her mother’s drug addiction. She learned to take care of herself. The loss of several family members combined with mom’s addiction and unavailability sent Vanessa and her sister into a crisis culminating in their removal from the home. The family seems to now be on a positive track as the mother is in recovery and the girl’s have made improvements. However Vanessa understandably still has difficulty trusting her mother and other adults, and does not let adults help or guide her.

4. Latasha’s symptoms and level of functioning seem consistent with her admission diagnosis of Reactive Attachment Disorder, Posttraumatic Stress Disorder, and Oppositional Defiant Disorder. She experiences chronic and pervasive shame as a result of her past abuse, separation from family, disruptions from foster care, and multiple placements. These feelings of shame are overwhelming and cause her to react with a well-established pattern of oppositionality and defiance. In addition, considering that her developmental stages were disrupted by her trauma, she may be struggling with issues of competency and trust leading her question her own safety and sense of belonging as well as her ability and to learn new skills and grow in her functioning.

Latasha will benefit from the routines and structure of daily living in residential treatment. Latasha will benefit from a restorative approach in treatment to help her gain confidence and trust in her caretakers and to allow her to develop her strengths, which include good verbal skills, a sense of humor, and an ability to engage positively others, in the context of healthy relationships.

5. Stephanie is a bright and insightful child who has suffered immense abuse and neglect in her formative years. She was witness to horrendous domestic violence, substance abuse and sexual activity. Stephanie was often the caretaker of her brother and biological mother while her own needs went unmet. As a result, she learned that it was not safe to trust adults to care for her. Upon her adoption to the Anderson family, Stephanie struggled to adjust to this environment. Her adoptive parents appeared to accept her need to be in control and for a while went along with her behavior. However, over the years, Ms. Anderson grew increasingly worried and angry. As she became more vigilant in monitoring her daughter, Stephanie grew increasingly oppositional and detached. Ms. Anderson felt Stephanie was deteriorating and influencing her other children whom she felt were connected and settled. As a result, Ms. Anderson gradually began to disconnect from her daughter. Stephanie impacted by fears of abandonment responded accordingly and became increasingly withdrawn and detached from the family.

Ms. Anderson raises her foster and adoptive children primarily on her own without much spousal support and is looking to meet her needs through her children. Her husband is largely unavailable and detached. She expects her children to “love back” considering how much effort she puts into caring for them. Stephanie’s lack of attachment to her, therefore, is intolerable. It is also complicated by the fact Stephanie is entering adolescence. Ms. Anderson has limited experience with this stage of development and since her own childhood was unremarkable, she expects the same from her children. Ms. Anderson is also angry at Stephanie due to the conflict it has raised with her own parents, who criticize her parenting skills and lack of nurturing with Stephanie. Her perception of their withdrawal of support has been extremely painful, which she blames on her daughter. Ms. Anderson feels that she needs a break from this child and treatment will focus on whether the relationship can be restored in order to support Stephanie’s return home.

The formulation articulates our theories, our understanding of what causes problem behaviors and what helps to heal them. The formulation leads directly to the treatment plan. In the treatment plan we describe the problem behaviors, we describe their positive opposites, the behaviors we would like to see, and we describe the steps to get there. The treatment plan, again, is a theory: it makes concrete our understanding of the steps that would help a child heal. Thus if Latasha is feeling shame, what will help her? Experiences of competency, positive relationships, identifying strengths, developing skills to master her own emotions. These should be clear in her treatment plan.

If Vanessa cannot trust adults and use their help, what will change that? Small experiments in trust. Using her leadership and self care skill to accomplish things. Positive trustworthy relationships. An understanding of her past and it’s effect on her. Developing emotion management skills to withstand the fear she experiences when she beings to trust.

If Stephanie and her foster mother are locked in a painful cycle of unmet needs, what will help? The relationship between the therapist and Ms. Anderson may begin to meet some of her needs, allowing her to relax with Stephanie. Perhaps her mother will be part of the family work. Helping mother and daughter share their experience and listen to each other may be part of the healing. Structuring positive experiences between them may begin to rebuild their connection. These interventions would be clear in the treatment plan.

So the clinician’s job is to gather information respectfully and understand the experience of the child and family, then to use that to develop a formulation. The formulation articulates what has happened, what is going on now, how these factors produce these behaviors, and what steps may help move towards more effective meeting of needs. Then, the clinician must convey this formulation to the entire treatment team, including the child and family (in understandable and respectful language).

Then, and perhaps even harder, the clinician’s job is to keep the formulation alive. Whenever a new behavior happens, or the four hundredth repetition of the old behavior, or an accomplishment, or something bewildering, return to the formulation. Is this still how we understand this child and family? Do we need to adjust our thinking? How do the new events fit into our theories? Where does this understanding lead us- what new interventions are suggested?

For this to be a viable and vibrant process the clinicians need administrative support. They need excellent clinical supervision. They need access to on going training of many sorts. They need opportunities to replenish them selves and their work. They need reasonable caseloads which allow time to think about their kids.

This clinical leadership will gradually develop a more knowledgeable and sophisticated team, in which all the staff will assume the child is doing the best they can, routinely wonder what is behind a behavior, and seek ways to help the child develop new skills. This thinking will produce more creative and caring intervention possibilities. And this will lead to more deep and lasting healing for the children and their families.

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Beauty Buzz: New Makeup Autumn 2008 Part 3

Estee LauderMakes us crave for chocolate with their Autumn Collection in chocolate colours! Yum!The collection inlcudes: Estee Lauder Signature Eyeshadow quads- 4-colour eyeshadow palettes (come in 2 tones chocolate/caramel browns and berry tone), Creme Caramel Shimmer Powder, Swirl lip gloss (cramel and berry tones), Longlasting Lipstick (in Berry Swirl and Varamel Swirl)I definately have to

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ADHD gene #5: Serotonin transporter gene (5-HTT)

ADHD Genes

ADHD Gene #5: Serotonin Transporter Gene (5-HTT, also referred to as "SLC6A4"): 5-HTTLPR long allele, location 17q11.1-12

This is the fifth gene that is being discussed on our list of ADHD genes. If you are not familiar with some of the terms in this post, here is a section on background information as it pertains to our study on ADHD genes. For a list of the other ADHD genes, please click here. The Serotonin Transporter Gene is found on human chromosome #17 (the q11.1-12 refers to a more specific region on the chromosome, and is not important for the time being). As mentioned in previous posts, genes come in different forms or alleles. One of the forms, or alleles of the Serotonin Transporter (5-HTT) gene has been associated with an increased risk of developing ADHD.

It is important to note that the terms Serotonin Transporter Gene, 5-HTT, and SLC6A4 all refer to the gene as a whole. The term "5-HTTLPR" refers to a specific section or part of the gene that can vary from individual to individual. For more background information on how genes are structured, please click here.

When the results of several family studies was pooled statistically, individuals with the "long" allele of the gene ("long" refers a form of the gene that has slightly longer DNA sequence than the shorter form of the gene), had an increased likelihood of developing ADHD than those with the "short" allele of the gene. Nevertheless, there is still some evidence that the "short" form may be tied to a higher incidence of ADHD as well (however, the trend in evidence typically favors the "long" allele).

Based on three different studies, there is some preliminary evidence suggesting that this "ADHD gene" (5-HTTLPR long allele), may be linked to autism as well, but a number of more recent studies have failed to support this claim. Nevertheless, it is known that individuals with certain forms of ADHD may possess higher levels of the neurochemical serotonin, which is also typically seen at higher levels in autistic individuals. Keep in mind that the gene of discussion in this post, 5-HTTLPR, is responsible for transporting serotonin into cells, with the "long form" (the "ADHD form"), transporting more serotonin than the "short" or "non-ADHD" form.

Based on how the most recent classifications, definitions, and diagnoses of mental disorders are done, individuals that fall anywhere on the autistic spectrum cannot be labeled as "ADHD" or vice versa (i.e., an individual may be diagnosed as being one or the other, but not both). However, a number of individuals with ADHD exhibit a number of symptoms that overlap with autism as well as vice versa. Of potential interest, our gene of topic, 5-HTTLPR, is responsible for shuttling serotonin into immune cells called lymphoblasts. Lymphoblasts are essentially an early, immature form of lymphocytes, which play a major role in an immune reaction such as an invading pathogen or an allergic response. The "long form" or "ADHD form" of this 5-HTTLPR gene shuttles more serotonin into the lymphoblast immune cells than does the short, "non-ADHD" form.

Higher levels of serotonin in these types of immune cells have been tied to an increase in migraine headaches, something that is also seen at higher levels in ADHD individuals. However, at the time, the cause is thought to be due more to an improper serotonin breakdown and disposal in these immune cells than transport mediated by the 5-HTTLPR gene. Nevertheless, it is an observation of potential interest.

Serotonin transporters, such as 5-HTTLPR, are also thought to play a role in seasonal affective disorders and depression. Higher activity levels of serotonin transporter proteins are seen during the fall and winter months (when depression is typically higher) than in the spring and summer. Although this 5-HTTLPR is likely not the primary culprit, the "ADHD form" of this gene does result in an environment similar to the "winter blues". This is due to the fact that the longer "ADHD form" of the gene transports more serotonin into cells and away from the space in between the cells. The net result is lower levels of free serotonin, which is typically seen in patients suffering from depression. Not surprisingly, depression is seen in much higher levels in several types of ADHD when compared to the general population.

One caveat here: some of the comparisons here are meant to simply report on a potential genetic overlap among ADHD and other disorders or diseases (migraines, autism, depression, etc.). At this point, there is not enough information to adequately confirm that the "ADHD version" of the Serotonin Transporter gene being discussed in this post is the primary cause of some of these other disorders. However, keep in mind that some of the underlying mechanisms of action are very similar and should suggest further investigation.

ADHD genes

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Beauty Buzz: New Makeup Autumn 2008 Part 2

In this post: Guerlain and GivenchyGuerlain Guerlain’s look for Autumn 2008 is Femme Fatale. Enjoy limited edition of their Jeu de Dames (A GAME OF SEDUCTION) collection including KISS KISS JEU DE DAMES lip palette and 2 Ombre Éclat - Eyeshadow palettes. Don’t miss Guerlain's Blush 4 Eclats – a compact available in six various combinations of shades, ideal product for sculpting the face. Plus

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Improving Restorative Tasks

Three ideas have recently occurred to me related to making restorative tasks more meaningful to both kids and staff.

1. Mapping the Effects of Behaviors: In a workshop I just attended on Restorative Practices in a school the presenters emphasized that after each incident they meet with the child and create a map of who was affected by the child’s recent actions. Include any one who was affected positively! Then the child has a chance to think about how to make it up to them. Some children would be unable to do this because their shame would produce overwhelming and intolerable emotions. But for those who could, taking this step formally might be a way to underscore the meaning of the restorative tasks.

2. Practicing Positive Ways to Meet Needs: A key tenant of trauma informed care is the belief that symptom are adaptive, that every behavior is a person trying to meet their needs the best way they know how at that moment. The behavior (hurting yourself, running away, throwing a chair) may be an escape from intolerable feelings of despair and hopelessness. It may be a way to draw humans closer and avoid deep aloneness. It may be a mask for desperate fear or unacceptable confusion. But the behavior serves a function, and it helps in the moment. It actually makes things better for a time, even if it also brings long tem negative results.

Led by the clinician, the Treatment Team should try to understand the needs that this child’s behavior is meeting. They can do this by talking with the child, by noticing patterns, by knowing the child and her history, even by guessing. And then their job is to teach the child how to meet these needs in ways with less negative consequences.

So how about using the learning part of restorative tasks as ways to discover and practice these new ways of meeting needs? So Yolanda is angry and destructive many nights before bed, and the team speculates that night time is hard for her and she has trouble falling asleep due to racing unhappy thoughts. What if her restorative task is to read a story to a younger girl on the unit every night? Or (with staff help) to put together a CD of soothing sounds and make copies for some other girls whose lives she disrupted? Or to make a stuffed animal for someone filled with lavender- and make one for her self too?

Get the idea? Yolanda learns some ideas of how to fall asleep, while making amends to others.

What if we postulate that Andre becomes aggressive and assaults staff whenever he feels afraid. What would we like him to do when he becomes afraid? Probably tell some one. So how could he practice that? He could talk with three of the male staff about times they felt afraid, and what they did about it (experience modeling of the desired behavior). Could he read or write a story about a boy who was afraid and handled it well? What else occurs to you?

In treatment team, think about the needs a behavior is meeting and what the desired way of meeting those needs is. Then think of some possible ways the child could experience or practice that more positive alternative.

3. Peace offerings: In a novel I just read when one character hurt a friend, she brought her friend a peace offering when she went to apologize (I think it was cookies). It occurred to me that the concept of peace offering conveys what we want to accomplish in the making amends part of the restorative task. The things we ask the kids to do to make amends can never be as big as the things they have done wrong (at least, not if we want to stay licensed). So using the phrase "peace offering" might help convey the spirit of what we want them to accomplish- a gesture of apology.

Click on the comment button below and let me know your reactions to these ideas.

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Beauty Buzz: New Makeup Autumn 2008 Part 1

In this post: Chanel and LancomeChanelAutumn 2008 Chanel style is very gold and... very Chanel. Image: Chanel.comThe man behind the idea -Peter Phillips, Chanel's Creative Director for Makeup, was inspired by Mademoiselle Chanel's appartment "a unique place with golden covered walls and warm tones"I love this new makeup collection!LancomeLancome takes inspiration for Autumn 2008 look in

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Beauty Buzz: New Skin Care Products this Autumn

This autumn several new anti-aging products will become available for purchase in stores. Some of them mentioned below.Estee Lauder comes out with a new anti-aging serum – Perfectionist [CP +], Wrinkle Lifting Serum, Corrector for Lines/Wrinkles/Age Spots.It contains peptides that, as Estee Lauder promises, provide effective action against wrinkles, lift and restructure. They promise that in just

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Beauty Talk: Eye Puffiness

I was prone to under eye circles since I can remember. However, you can fix this problem with the help of a mask, a good eye cream and of course a good concealer. A month ago I faced a much harder problem – eye puffiness… mostly under eye puffiness… If I had a choice between the circles or puffiness I would go with the former. But I did not have that choice – so now I have to deal with both!

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How Much Restoration is Enough?

In a recent training I did, I was asked a familiar question: how do you know how much restoration is enough? When a child does something that hurts another person or threatens the community, how do you decide how many or how large the tasks assigned for restoration should be? And how do you decide whether the child has completed these tasks with enough sincerity, effort or seriousness?

I think that some of the impetus for this question comes from thinking of restorative tasks as punishments in disguise, and from believing that their effectiveness comes from their being aversive. In other words, that (like punishment) the tasks should not are fun to do, and the child will change his behavior in order to avoid having to do them. In this framework, the tasks should be "as big as" the offense, and take a lot of effort and time, especially if the behavior was very serious or hurtful. The learning or relationship nature of the tasks is secondary. People often speak of staff feeling like the child "got away with" his behavior because what he had to do was not hard enough. The person who was hurt by the child does not feel sufficiently paid back, and thus feels resentful and disrespected.

In order to think further about this, let’s turn to our own lives. We all have had experiences of forgiving people who have hurt us, and continuing the relationship. Imagine that a friend has done something that hurt you. What would that be? Told a secret, let you down, forgotten to meet you for a planned appointment, said something thoughtless or mean to you, cancelled a plan with you at the last minute in order to do something else, borrowed money and not paid it back: what else?

In order to restore this friendship and for you to truly feel better about this friend, what would you want from him? First, I guess, an apology and an acknowledgement of what went wrong and his part in it. You might want him to listen to you speak of how this behavior affected you and to seem to actually care and take in what you said. Then, you would want him to act differently from now on, or try to, or at least start to.

So these are the skills and behaviors we want our kids to learn.

The first thing that gets in the way is shame. In order for a person to deal directly with something they have done wrong, they have to be able to tolerate the bad feelings involved. In order to admit you have hurt some one and to face them, you have to have some inner core of believing you are okay. You have to believe that forgiveness is a possibility.

Stop here for a moment and think of a time when you did something wrong, hurt some one you cared about, or made a mistake you were ashamed of. As you were trying to convince yourself to face up to the mistake and deal with it, what were you feeling? What got in the way of your honestly going to the person you hurt and admitting what you had done? What helped you to do so?

When our kids realize they have made serious mistakes, their sense of hopelessness comes crashing down on them. All is lost. There is no hope of forgiveness or redemption. They remember everything that has gone wrong in their lives, which they believe is totally their fault. When feeling this horrible despair and seeing no way out of it, their impulse is to run away from the events. This running can take many forms: actual running, denying responsibility, blaming or attacking others, aggression, self harm, retreat to bed, and many others. Often it takes the form of the child demanding to get out of this stupid place: send me to detention! Hospitalize me! All of this reflects self loathing, despair and lack of hope.

So- back to the restorative tasks- in treatment we are trying to help the child grow and be able to feel hope, to believe in the possibility of things working out, and to have some skills that will provide steps towards that outcome.

Traditional punishment, such as confinement to your room for a period of time, has exactly the opposite effect- it leaves the child feeling worse and without any adult support or steps to reconnect with others.

The restorative tasks should aim towards helping this particular child, with her particular abilities, needs, and treatment formulation, to become slightly better at:

• Acknowledging what went wrong and her part in it.
• Listening to the hurt other speak of how this behavior affected them, caring and taking in what that person says
• Acting differently from now on

In order to do any of these, the child has to develop some sense of being a worth while person, someone who deserves the air she breathes; some one others could care about and could forgive. Much of our treatment is designed to accomplish this in many different ways.

How do you get better at acknowledging your mistakes, and listening to the other describe the effect on them? Practice, mostly I think, and discovering that the world doesn’t end and in fact you can often repair the relationship. So, for some child the whole making amends could be a short conversation with the person hurt- that could be a huge step for her. Another child can’t do that, the shame is too intense. But he can draw a picture of the steps leading up to the event, and how he was feeling, and give it to the person hurt. Maybe she could respond by drawing a similar picture of the events from her point of view and how she was feeling- and he could further respond with some communication that shows he paid attention to what she said. The goal here would be: what are this kid’s current abilities to face her mistakes, and what action would be one small step further than she usually can go? In the past in this child’s life, making mistakes has led to abuse, and often to the person hurt disappearing all together. Our goal is to make this time different, a restorative relationship experience, to create a new template which includes the possibility of healing.

We’d all like the kids to then act differently. Preferably completely and immediately. In fact, that is one difficulty people report with the Restorative Approach- when you engage in a heart felt exchange with a child and the child still repeats the behavior, it feels worse than when you punish them and they repeat the behavior. We all know it takes a long time for these children to change, to un-learn the lessons of their life times.

But what will it actually take for the child to be able to behave different? Emotion management skills. Developing a sense that there are people who care about him, and that thy still exist when they are not physically present. Developing a sense that he is worth the air he breathes. And developing the ability to recognize, name and manage emotions, including the ability to self-sooth.

Thus, the learning aspect of the restorative tasks. This part is aimed to teach some small part of emotion management skills. This could be describing what I was feeling, or what else I could do, or listing ten good things I have accomplished, of drawing pictures of people who care about me. Again, what are this child’s current emotion skills strengths and deficits? What are the next steps in her treatment, what are we currently trying to teach her? Let’s give her some chance to practice as part of her restoration.

So back to the question we began with- how much is enough? It is enough when the staff feel the child has made any little step on any of these dimensions. They have talked about what happened sincerely. They have actually listening to the person they hurt. They have explored the feelings that led up to their actions. It doesn’t have to be the whole solution- just one tiny step, one new interpersonal experience, one moment of feeling "I am worth worrying about"- one building block in creating a new reality for the child.

Next questions- how do we as a team decide this? How do we teach it to new staff? How do we convey it to the children? Let me know your thoughts.

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ADHD Gene#4: Dopamine Beta Hydroxylase Gene (DBH)

ADHD Genes


ADHD Gene #4: Dopamine Beta Hydroxylase Gene (DBH), Location: Chromosome 9 (q34)

Dopamine Beta Hydroxylase (DBH) is the fourth gene on our list of ADHD Genes. For humans, it is listed on the 9th Chromosome ("q34" refers to a the specific location on the chromosome for the gene). For a list of the other ADHD genes that are being discussed, please click here.

What makes this DBH such an interesting gene associated with ADHD is the fact that several diseases or disorders that are often comorbid (existing alongside of or with) ADHD also have ties to this gene. Among them are smoking (both in tendency to smoke and the number of cigarettes smoked per day) and suceptibility to migraine headaches. Additionally, there is a suggested genetic linkage between a particular form (allele) of this DBH gene and a built-in resistance to Parkinson's disease. Of somewhat interest is the fact individuals with ADHD are statistically more susceptible to contracting Parkinson's later in life than the rest of the general population.

In studies with mice, an analogous DBH gene has shown to play a strong role in regulating body temperature as well as being a key component in response and sensitivity to common antidepressants including Prozac, Paxil and Zoloft.

A major function of the Dopamine Beta Hydroxylase (DBH) gene is to produce an enzyme of the same name, dopamine beta hydroxylase. This enzyme is responsible for converting the important nervous system chemical dopamine into another important chemical called norepinephrine. Individuals with ADHD often show abnormal levels of one or both of these chemicals (typically on the low side). For this enzyme to function properly, it requires adequate levels of the mineral copper as well as ascorbate (a form of Vitamin C). Deficiencies in either of these two dietary components inhibit this enzyme's effectiveness and produce similar symptoms to a DBH deficiency. It is therefore advisable that ADHD individuals take in adequate levels of both of these key nutrients (roughly 2 mg/day for copper for the average person and at least 60 mg/day for vitamin C).

However, even with adequate intake of these two nutrients, ADHD symptoms can definitely persist. One of many possible causes could be an inherited form of the DBH gene that is statistically linked to ADHD. This can be determined by a personal genetic screening. One allele (form) of this ADHD gene is called the DBH A1 allele. Several studies have shown that there is a significant association between this A1 form and ADHD.

In addition, there is some evidence that another allele (form) of this DBH gene on the 9th human chromosome may also play a role in developing ADHD. This form is called the DBH A2 allele. Although there is a somewhat weaker association between this form of the gene and ADHD than the A1 form, several family studies have shown a notable correlation between the presence this form of the gene and the development of ADHD. Additionally, some research has suggested that the presence of this A2 form of the gene is tied to a parental history of ADHD (often with a higher correlation to the father), and the subtype of ADHD. Some evidence (which has not been repicated extensively) points to a correlation between this A2 form of the gene and an ADHD subtype called the combined subtype.

The combined subtype refers to a subtype that encompasses both the inattentive component and the hyperactive/impulsive component. The inattentive component has been tied to two other "ADHD genes" previously discussed, the DRD4 gene, and the DRD5 gene, while the impulsive/hyperactive component of ADHD which has been associated with another previous post of a gene and its "ADHD form" called the DAT gene.

The next post will soon be up on another "ADHD gene" of topic, the Serotonin Transporter Gene (5-HTT).

For a list of other posts on ADHD Genes, please click here.

ADHD genes

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ADHD Gene#3: DAT

ADHD Genes

ADHD Gene #3: Dopamine Transporter Gene (DAT, SLC6A3), Human Chromosome #5

There have been a number of recent postings on genes thought to be connected with ADHD. Previous ones discussed include the ADHD form of the Dopamine D4 receptor Gene (DRD4), the ADHD form of the Dopamine D5 Receptor Gene (DRD5), and, to a lesser degree, the DRD2 ADHD gene. However, one of the most intriguing ADHD genes is a gene called the Dopamine Transporter Gene, abbreviated as DAT. An ADHD form (also called allele), of this gene, which is located on the 5th chromosome in humans, has been tabbed. The ADHD gene DAT has been discussed in another recent post, where it has been tied to a mutated form of a protein called the dopamine transporter protein that "shuttles" an important brain chemical, called dopamine, in and out of neuron cells. While the regular form of this protein functions, normally, the mutated form causes it to run in the opposite direction at high speed, significantly changing the distribution of the dopamine chemical throughout the brain. This balance can result in extreme ADHD symptoms, and has also been seen in bipolar individuals.

Statistically speaking, there is a weaker correlation between the above form of the gene and ADHD behavior than the previous two genes. Nevertheless, this gene serves as an important target for stimulant medications (such as Ritalin) for both rats and humans. A number of studies have been done on an analogous gene in mice has shown that altering this gene function resulted in a noticeable increase in hyperactivity and decrease in behavioral inhibition and control.

Remember, two ADHD genes mentioned in previous posts, the DRD4 ADHD gene, and the DRD5 ADHD gene are both thought to be more affiliated with the inattentive component of ADHD. In contrast, individuals with the DAT gene mentioned in this posting, above are more prone to hyperactivity and behavioral inhibition problems associated with ADHD. We will soon discuss the various components and subtypes of ADD and ADHD in later posts, but for now, please keep in mind that a number of different genes may be at work within and ADHD individual.

There is still a fair amount of research to be done on this gene, but for now, we can cautiously assume that there is a correlation between forms of this DAT gene, located on the 5th human chromosome, and ADHD.

ADHD genes

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Beauty Brand: Guerlain

Guerlain is one of the oldest perfume houses in the world. It was founded by Pierre-Francois Pascal Guerlain in 1828 and and since then more than 300 perfumes were created by this famous house.Pierre-Francois started from opening a perfume store on 42, rue de Rivoli in Paris. Beginning of Guerlain’s long history of success was marked by Pierre-Francois aquiring the title of Her Majesty’s

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ADHD Genes: DRD2

ADHD Genes

Dopamine D2 Receptor Gene (DRD2): TaqI A1 allele, chromosome 11 q22-q23

Based on the same overview study (Faraone and Khan, J Clin Psychiatry 2006; 67 (sup 8), 13-20) as the other seven ADHD genes, there has been some association between a gene on the 11th human chromosome and likelihood of developing ADHD. The form (also called "allele") of this gene associated with ADHD is called the Dopamine D2 Receptor Gene (DRD2) TaqI A1 allele. The findings from the main study on this gene were not replicated, but one study found that individuals possessing the above form of the gene showed an increased likelihood of having ADHD.

Interestingly, this form of the gene is also associated with at least two other disorders that are known to frequently occur alongside of ADD and ADHD. Individuals carrying the TaqI A1 form of the gene also showed a significant increased likelihood of having Tourette’s disorder. Tourette’s is a relatively common comorbid (meaning “occurring along with” or “occurring along side of”) disorder of ADD or ADHD. For those not familiar with the disorder, Tourette’s is a disorder that can result in involuntary behaviors such as “tics”, involuntary twitching, and, in some cases, outbursts of inappropriate speech and profanity. Along with ADD and ADHD, Tourette’s is also seen alongside of other disorders such as Obsessive Compulsive Disorder (OCD) at relatively high frequencies.

In addition to Tourette’s, there is evidence has linked the TaqI A1 form of DRD2 to Parkinson’s Disease (Grevle, et. al, Allelic association between the DRD2 TaqI A Polymorphism and Parkinson’s disease, Movement Disorders 2001, Volume 15, Issue 6, 1070-74). Several findings have pegged ADD and ADHD individuals to having a higher likelihood of developing Parkinson’s later in life. There is a distinct possibility that this form of the gene may be a significant underlying factor between the two disorders.

ADHD genes

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ADHD Gene #2 DRD5

In another post, I described that there were at least 7 well-known genes that are associated with ADHD. In fact, since the publication of this paper, additional ones have been identified. Within the past couple of months, another key study on ADHD genes has been discussed.

ADHD Gene #2: Dopamine D5 receptor gene (DRD5): CA repeat, 148 bp

In a previous posting, we discussed an ADHD gene found on the 11th chromosome in humans, called the DRD4. One of the forms (also called alleles) of this gene was associated with the disorder of ADHD, in particular the inattentive component of ADHD.

A second ADHD gene called the "Dopamine D5 receptor gene", or DRD5, is also thought to have strong familial ties to the disorder. Like the DRD4 gene listed above, DRD5 has multiple forms (or alleles). This is located on chromosome number 4 for humans. The "ADHD allele" which is referred to as "CA repeat, 148 bp" (this notation is commonly used by geneticists and refers to the length and DNA makeup of the "ADHD form" of the gene, the exact details aren't entirely important) is slightly greater in length than the non-ADHD form(s). While different studies on this allele have produced different results, it appears that this form of the gene, like the form of the DRD4 ADHD gene listed above, is tied more towards the inattentive than hyperactive component of ADHD. Statistically, however, there appears to be a weaker association between the DRD5 gene and ADHD than the DRD4 gene.

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