Tuesday, December 24, 2024
Home Blog Page 12

Integrative Psychiatry: Mental Symptoms and Nutrients

One of the benefits of visiting a psychiatrist who also specializes in holistic, complementary or alternative medicine is that he or she can determine whether or not a nutritional deficiency is the cause of some mental symptoms. Nutrients play a critical role in mental health. They are the building blocks of the nervous system. In fact, the brain has first call on the available supply of nutrients. Therefore, the first effects of nutritional deficiencies are often mental symptoms. Deficiencies in almost any of the vitamins and minerals can show up first as emotional or mental symptoms, such as depression, anxiety, or impaired memory and concentration. For example, folate deficiency is a common occurrence in psychiatric disorders, whether organic or functional, particularly in depressive illness.

There are specific nutrients which cause mental symptoms when that nutrient is lacking:

Calcium: Depression, delusions and irritability.

Chromium: Anxiety.

Copper: Depression.

Folic Acid: Apathy, depression, insomnia, paranoia.

Iron: Depression.

Magnesium: Anxiety, confusion, hyperactivity, nervousness, restlessness.

Niacin (B3): Confusion, depression, emotional instability, irritability, memory impairment.

Pantothenic acid (B5): Depression, irritability.

Potassium: Depression, insomnia, mental impairment, nervousness.

Pyridoxine (B6): Depression, irritability.

Riboflavin: Depression, nervousness.

Thiamin: Confusion, irritability, memory loss, nervousness. Individuals with a thiamin deficiency can develop Wernicke-Korsakoff syndrome, which is characterized by confusion, mental changes, abnormal eye movements, and unsteadiness that can progress to severe memory loss.

Vitamin B-12: Depression, irritability, dementia, mental disturbances, moodiness.

Vitamin C: Depression, irritability.

Zinc: Depression, irritability, lethargy, memory impairment, paranoia.

Omega-3 Fatty Acids: Depression.

Low Cholesterol: Depression.

There are three amino acids that are most directly related to mood and depression: phenylalanine, tyro-sine, and tryptophan. Phenylalanine and tyrosine produce the neurotransmitter norepinephrine, and tryptophan is eventually converted to serotonin.

Research has proven the effectiveness of amino acid therapy in fighting depression. Both phenylalanine and tyrosine-which is created in the body from phenylalanine-have been found to be as effective as the antidepressant drug imipramine. Phenylalanine has also been shown to reduce pain by preserving brain levels of endorphins, the body’s natural painkiller. Tyrosine is helpful in the treatment of PMS and chronic fatigue syndrome. Tryptophan, which the body converts into the precursor 5-hydroxytryptophan (5-HT), has also been found to be as effective as the synthetic antidepressants. (Cass)

Correct testing and understanding of deficiencies or overloads can pinpoint the causes of many mental symptoms, thus opening the door to hope and recovery. Positively demonstrating that nutrient supplementation improves mental disorders and proving that mental disorders are in fact due to nutritional deficiencies is difficult, however. Much research needs to be done to further explore this area.

Sources

Goldberg, Ivan, M.D. A Medline Search. “Folate, Vitamin B-12 and Depression“.

Wipond, Rob. “Healthy Brain, Happy Mind”.

Kapllan, Bonnie. “The Relationship Between Nutrition and Mental Disorders“.

Cass, Hyla M.D. “Nutritional Approaches to Mental Health“.

Thanks for installing the Bottom of every post plugin by Corey Salzano. Contact me if you need custom WordPress plugins or website design.

Facts about the brain

Your body contains at least 60 trillion cells.Yet your brain contains ‘only’ 60 billion cells, just 0.001% of the total. Proof that the ‘mind’ isn’t just inside your skull.

Each cell carries, on average 7000 connections to other cells. Therefore the number of cell networks in the brain is 42 thousand billion, or 42,000,000000,000 pieces of information your brain can, store.

Yet your brain only weighs 3 pounds and uses just 10-23 watts of energy per day. That is less than the energy in three bananas.

Each year you will lose about 3.3 million brain cells. But that is less than 0.00000006% of the total. And nearly all of it is replaced, right on up until old age.

There is no truth in the myth that we only use 10% of brain power. The entire brain is being used every day, even if some areas of the brain are there only for storage or for back-up functions.

Super memory. The brain is capable of storing 10 trillion bits of information about you and your life experiences.

The brain can make its own ‘heroin’. Endorphins are released in the Hypothalamus after vigorous physical exercise, injury, meditation, laughter and chocolate. Endorphins are up to 19 times stronger than morphine. By contrast, heroin is only 7 times stronger than morphine.

Being happy is good for the brain. Happy states trigger dopamine release, a feel-good chemical. Personal fulfilment increases neuroplasticity, slows down ageing and improves memory.

Why is adolescence so difficult? One main reason is that, between puberty and early adulthood, the brain is being rebuilt. There is massive growth in the pre-frontal cortex (Headmind); connections between cell networks are being hard-wired (making emotional life-lessons more intense); and there is a temporary loss of connection between the brain’s emotional centres (the limbic system) and the intellectual centres – which means that teenagers lack the capacity to make good decisions.

New experiences are vital for improved brain function. Getting out of the rut and going for new horizons increases cell growth, delays ageing and improves cell connectivity. The same goes when you let go of the past and exercise forgiveness.

Binge-eating. Emotional self-neglect can lead to food cravings and over-eating. So-called stress triggers an increase in Cortisol in the blood stream, which stimulates Insulin release. High insulin levels are associated with a craving for sugary foods and foods high in carbohydrates.

Regular sex (at least twice a week) improves daily moods, reduces pain thresholds, cuts the risk of a heart attack, decreases menstrual pain and promotes sleep. This is because enjoyable sex fosters highendorphin release.

Love and sex can be addictive. Falling in love, like sexual infatuation) is similar to taking cocaine: the hypothalamus triggers a cascade of dopamine. One problem is that, once the dopamine wears off, a ‘down-mood’ sets in, leading to further cravings.

The brain also contains a bonding chemical: Oxytocin. During labour, female brains produce large amounts of oxytocin, which stimulates contractions and smooths the passage of the baby down the birth canal. Oxytocin also creates a primal, intense bond with the child. Adults in love (or during ecstatic sex) also release high levels of oxytocin.

Thanks for installing the Bottom of every post plugin by Corey Salzano. Contact me if you need custom WordPress plugins or website design.

The Ten Biggest Mistakes Psychiatrists Make

1. Talk too much
It’s not a conversation, and it’s not a debate.  You are either treating their symptoms with medication, or guiding them to “treat” their own symptoms.  Neither requires much talking.

If the psychiatrist says more words than the patient, then the psychiatrist is the patient.

Many psychiatrists talk because they feel powerless.  The patient is in distress.  How can the session be worth the money unless they get some thing?  A prescription is good, but what else—what now?  So the psychiatrist thinks they need to say something, to appear as though you are giving something to the patient.  The worse the situation is, the more the psychiatrist talks.  You’re talking to make yourself feel better, to justify your value as a psychiatrist.  Don’t do this.  It’s not help.

And empathize, don’t sympathize.  I cringe whenever I see a psychiatrist on the first visit  try to sound genuine while they affect a sad and shocked voice, lean forward, grab a box of tissues, “oh my God, I’m so sorry, that’s terrible!”  It’s fake, which makes it annoying, but it’s patronizing, which makes it countertherapeutic.  A psychiatrist cannot sympathize—did the same thing happen to you?.  What they need to do is empathize, to understand the feelings, to appreciate them—not to share them.  Plus, you don’t know what the situation means to the patient.  Maybe they’re secretly happy (and guilty about it), and now that you’ve confirmed that it’s “terrible,” they’ll never admit to you or themselves they’re happy about it. Simply saying, “I’m sorry.  Can you tell me more about…” is all that’s necessary.

And enough with the tissues.  If you stalled the interview to go get them a box of tissues, you have failed, you changed the energy of a key moment. And you did this—let’s be honest—not because they needed tissues, but because it took some pressure off the moment and allowed you to give them something.  Leave tissues by the patient chair from the beginning, and focus on what you’re doing.

I had a great mentor who taught me to begin the first session with the words, “Where would you like to begin?”  And then to shut up.  Great advice.

2. Take too much history

This is going to be controversial.  I can hear academics seizing.

I know psychiatrists are taught that careful, meticulous history taking is the cornerstone of good care.  Well, it’s not.

Every session should be about the patient, not about you.   You’re supposed to help them, not understand them.  The two may go together, but they might not.    It is possible for you to help without understanding, but it is not acceptable for you to understand without helping.  You’re not CSI, you’re not Batman, you’re not trying to solve a mystery or make some aha! discovery.  They’re telling you what’s wrong.  Just listen.   Taking a detailed history may seem like a good idea, but many times it is masturbation, it contributes nothing to the patient’s well being, it only makes us feel thorough.  As in: well, I can’t do much for him, but I got a really good history.  Remember, it’s not about you, it’s about them.  It may seem as if a strong family history of bipolar disorder is important information, but it isn’t.  I know, bipolar runs in families and blah blah blah. You couldn’t tell they were bipolar before you learned their family history? And how do you know the family’s diagnosis was correct, so that you can rely on it to make your diagnosis?
I’m not saying don’t get the information.  I am saying devoting the first one or two sessions exclusively to this gains the patient nothing.  Everything from the moment they walk through the door should be about their service.  Forget about the notes, especially outpatient notes.  Worry about the patient, the notes should come second.

Are you proud of your notes because they contain so much detailed patient information?  You need to think about this.  Did you break eye contact to write, “sad over husband’s loss?”  Then you missed the moment.  Just listen—write your notes after the session.  And if I see one more  psychiatrist with a note pad playing stenographer I am going to punch him in the neck.

3. Ignore smoking cessation

or at least make it a secondary outcome.  Also applies to soda/juice/calorie reduction.

This may seem trivial.  It’s not—after the treatment of the initial presenting acute symptoms and treating drug and alcohol abuse, this is more important than almost anything in psychiatry.  The logic is as follows:

1. Smoking is obviously and severely detrimental to one’s health, arguably more damaging than hypertension and depression combined.  Its effect on life expectancy rivals, well, arsenic.

2.  It is an addiction, so it is psychiatry’s business.

3.  It is highly comorbid with psychiatric disorders, and may be a relative symptom of them.  (For example: half of all people who commit suicide smoke.)

4.  Smoking itself has a significant impact on other medications (e.g. did you know it reduces Haldol by half?)

5.  What the hell else are you doing with the session?   Especially in the “maintenance” phase of psychiatric treatment (where symptoms are relatively controlled, etc).

All of this applies equally to soda consumption or even diet in general. Drinking 2 liters of soda a day may not seem like a psychiatric issue, but most of the medications used have the propensity to increase appetite, and excess eating, smoking, soda drinking are hardly psychologically meaningless behaviors.  If your psychiatrist asks you to keep a mood chart or teaches you about “serotonin dysfunction,” but doesn’t tell you to quit smoking, run.  He has missed the forest for the trees.

 

4. Blame lawyers/insurance companies/Big Pharma
In order to understand why this is such a popular mistake among psychiatrists (all doctors, actually) it’s useful to identify when psychiatrists do this.  There are two specific times.  The first is when psychiatrists seek to justify doing, or not doing, some clinical maneuver, as in, “I can’t discharge him from the emergency room, even though I don’t really believe he is suicidal, I think he is lying simply to get hospitalized– but I don’t want to get sued.”  The second time is when psychiatrists seek to explain a reduction in income, as in, “The insurance company only pays so much for a visit, so now I do only med checks.”

What is striking about these justifications is that they almost never relate to the specific problem at hand, they are scapegoats for some general anger about the difficulty of practice.  For example, in the example of the malingering emergency room patient, discharging him has no increased risk of legal liability because if the patient is, in fact, malingering, then he will not kill himself.  The operational issue here is not one of increased legal liability, but whether a physician can detect malingering.  This has nothing to do with lawyers.

In the second example, while it is certainly true that the insurance company has set reimbursement rates, psychiatrists have not explored their responsibility in this.  They have not, in any scientific, economic, and most importantly policy way, justified the necessity for a different (read: higher) reimbursement scheme.  Consider psychiatrists’ attitudes towards psychologists acquiring prescribing privileges.  It seems obvious that psychologists shouldn’t prescribe medications, but why not, exactly?  To say that psychiatrists are trained in medicine and better understand drug-drug interactions, dosing, and toxicities presupposes that the average psychiatrist actually does know about drug-drug interactions, dosing and toxicities.  Really?  What’s the interaction between Prozac and hydralazine? Don’t know?  Then why should psychologists know?  And if you can look it up, so can they, etc, etc.  Also, using this reasoning could backfire, as it can justify an insurance company refusing to pay for a psychiatric med check since the service could be performed by a primary care doctor (who will also handle everything else for the same low price.)  Again, it is easy to complain, but it is on psychiatrists to explain, rationally, why it should not be.

Consider the common complaint that each insurance company has its own formulary, requiring doctors to prescribe alternatives, generics, or submit prior authorization requests.  This is taken as bureaucratic interference of patient care.  However, in the majority of the cases these restrictions are economically and clinically valid.  No logic, let alone evidence, exists for prescribing two antipsychotics simultaneously.  So why should the insurance allow it?  Similarly, an insurance company should be allowed to approve drugs based on cost, because unless one can show that, for example, two SSRIs do not have the same general efficacy or tolerability across a population, than an insurance company cannot be reasonably obligated to provide both, especially if it can contract to receive one of the SSRIs at a cheaper cost.  To be clear: it may, in fact, be true that (for example) two antipsychotics are better than one.  But the burden of responsibility is on psychiatrists to show that this (or any clinical) maneuver is necessary, and not on the insurance companies to simply trust that doctors know best, because they have shown repeatedly that they do not.

Blaming lawyers has almost become a sport.  It is certainly true that uncapped awards for damages hurts everyone (except lawyers.)  However, lawyers are good at picking  malpractice cases, not at inventing them. Consider informed consent: if one prescribes valproate for maintenance, one must not only discuss the side effects, but also the alternatives to treatment– especially when the alternatives to Depakote (a drug which has neither approval for maintenance nor rigorous data backing it) do have such approval and data  (consider lithium, Zyprexa, Lamictal, etc.)  To prescribe Depakote because it is at the top of an algorithm or in the “guidelines”, or because “that is my practice” and not because of a reasoned analysis of theindividual merits of the case, is at minimum not thoughtful practice.  A similar example is psychiatry’s current obsession with antipsychotic induced diabetes.  Assume that Geodon does indeed have a much lower risk of diabetes than Zyprexa; is a psychiatrist any less liable if the diabetes is induced by Geodon and not Zyprexa?  No.  You don’t get sued for using Zyprexa.  You get sued for causing diabetes and never picking it up.

To state explicitly what seems the most obvious point of all: if a medication causes a side effect, and you catch it, there’s no lawsuit, because there’s no damage.

The above examples come from misunderstanding the available scientific literature, or not knowing it at all.  Oddly, if a lawyer does not research the current state of case law and statutes before answering any legal question, it is legal malpractice.  But doctors practicing medicine are not required to review current journal articles on any medical condition.

Pharma is the most maligned of all.  On the one hand doctors resent the intrusion of the industry on their practice; on the other hand, industry is the primary—often only–  ongoing educational source for doctors, whether they believe this or not.  Drug reps, throwaway journals and supplements, “drug dinners” and almost all CMEs (yes, CMEs  too, stop lying) are all industry sponsored educational processes which are the de facto continuing education of most psychiatrists.   Oh, right, right–  doctors learn by regularly reading numerous journals carefully and thoroughly.  Ok–ask them to name one article in the most recent issue of the American Journal of Psychiatry.  Not the results of the study; just the title.

One may want to ask why the FDA feels it necessary to hold pharmaceutical reps to extremely strict standards: they cannot mislead, they cannot speak off label, they must discuss side effects and toxicities, and they cannot use any promotional material that was not reviewed by the FDA.  Used car salesmen are not held to any standards, and they sell to idiots.  No one needs to tell you the rate of blowouts on a Firestone tire.  Why would doctors—the most educated consumer group in existence—need protection from salespeople?  Shouldn’t doctors, ultimately, know more about the medications than the sales reps do?  Unless…

The sad truth is that the state of psychiatry is the fault of psychiatrists, who have failed to take full responsibility for their own education and practice.  To blame anyone else at this stage is remarkably disingenuous.

 

5. Become social policy analysts
Remember how in May, 2005, the American Psychiatric Association endorsed same sex marriage?   And you applauded the moral fortitude and progressive instinct of this august body?  Well, instead of debating whether there should or should not be same-sex marriage, perhaps we should ask what modern psychiatry could possibly contribute to this discussion. The answer is nothing.

You can’t get away with pat answers, such as psychiatrists see the psychiatric ramifications of discrimination or being unable to marry. There are psychiatric ramifications of bankruptcy, and war, but no one felt compelled to write a policy statement on it (and thank God.)

And no, there isn’t a difference between bankruptcy and gay marriage– not to psychiatry. That’s the point. These are social problems about whichmodern psychiatry is definitionally ignorant. The APA did not endorse polygamy. What’s the difference? If homosexuality is not a psychiatric disorder, than there is no more reason to be more for or against it than there is for any other kind of marriage. The APA is no better suited to answering these questions than, say, the NFL.

What if the NFL came out against antidepressants in children? This is a perfectly valid analogy, because neither the NFL nor psychiatry have special knowledge that make their statements anything more than opinions. What do psychiatrists know about same-sex marriage that the quarterback for the Patriots doesn’t?  Don’t laugh—I’m serious. What’s the answer?

Medicine, or the APA, can legitimately express a policy only if  the policy was grounded in science or logic. Perhaps the APA cares to release this intriguing scientific data?  (While it is at it, perhaps it can also release the data supporting the use of half of the medications currently favored by APA Guidelines?)  But this seems pretty much business as usual for the APA. Rather than work on its own serious failings, it involves itself in social policy.

“Modern” (read: pharmacological) psychiatry is obsessed with reinventing itself as a biological and scientific discipline. Well, if it wants to be a science, it better start acting like one.

The FDA effectively killed Vioxx, and not a peep was heard from the APA about the dangers of letting the government regulate their practice. You can say Vioxx has little to do with psychiatry, but it’s still a lot more than gay marriage.

Determining what is true and what is not, through serious and often disconcerting scientific enquiry, is very difficult. It is much easier to involve oneself in matters of opinion and debate, in activism, because it is both immediately rewarding and it is easy. It’s hard to measure things in psychiatry, and when it is possible the results are often disappointing. So it busies itself with matters of conviction because it feels some responsibility to have convictions. It doesn’t. It has a responsibility to the truth, and if it doesn’t want to invest any energy in that pursuit, it is on them. But don’t mask it with whimsy and dilettantism.

I should point out that gays, far from being pleased with the APA’s stand, should actually be horrified.  Do you– does anyone– want social policy suggested by psychiatrists? Think long and hard.

Imagine the outrage if the APA had come out against gay marriage, or forthe war in Iraq. There would be battalions of people saying, “well, what the hell do psychiatrists know about war in Iraq? Who the hell do they think they are telling gays not to get married?” There is no protection in being confident of the rightness of your current position, as history is loaded with examples of how terribly bad doctors are at determining what is right and what is wrong. Not long ago homosexuality was considered a disease. See? The Tuskegee experiments were endorsed by the AMA, and the AMA gave its endorsement,  after ethics concerns were raised by Peter Buxtun. Remember that?  How about the speech to the1941 APA meeting, and the1942 issue of the American Journal of Psychiatry in which euthanizing the “feebleminded” (IQ<65) sounded like a good idea?

Psychiatry would do well to remember Wittgenstein TLP 7: Whereof one cannot speak, thereof one must be silent.

6. Don’t refer to therapy.

Psychopharmacology without therapy is treating an infection with Tylenol.

Medications do not cure a psychiatric disease; we’re not even sure what the disease actually is.   What they can do is reduce symptoms, give you strength—so that you can learn new behaviors.  That’s the point of medications.  Treating depression with an antidepressant is not the solution; it’s the preliminary step in allowing you to figure out how to handle depression later on.  The adaptation, the adjustment, the physical altering of brain functioning is done by new learning, often this is therapy (though it doesn’t have to be.)  I’m not saying therapy is that great, or necessary, either.  I’m simply saying that trying to improve a person’s long term status using medications alone without some sort of education and training is a waste of time.  It is maybe the most profound disservice of all to tell a patient that their depressive or bipolar symptoms are the result of biology or chemical imbalances and thus absolve them of the responsibility of learning new ways of interpreting and coping with their environment.

 

7. Don’t think strategically.

Psychiatry is fun, I’m sure, but it doesn’t help anybody when the patient refuses to play.   Psychiatry telling us opiate abuse is a heritable disorder related to polymorphisms in dopamine receptors doesn’t stop your kid from stealing your money to buy smack.  See?  Sometimes you have to hide your wallet.

What is the goal? What do you have to do to achieve that goal? Sometimes you have to look beyond the DSM.

Do what you have to do.  When a person needs treatment but is refusing it, neither the law nor psychiatry can help them.  I can’t force someone into treatment.  But you can.  Take drug abuse: in my experience, the only way to get someone to (albeit reluctantly) accept treatment is a large scale intervention.  10 people, minimum, in a cramped room with the future patient trapped as far form the door as possible, all ten  in energetic agreement that the person needs to get help– now.  Not tomorrow morning.  Immediately.  You’ve already packed his bags.   This isn’t a five minute pep-talk—take the whole day off, you’re going to be there a while. Also, a psychiatrist cannot do this for you, he shouldn’t even be there, because no one ever listens to neutral third parties, much less psychiatrists. (And I’ll just say it: you probably don’t want a psychiatrist there in case you…have to take things… to the next level…) It has to be ten highly motivated, concerned people.  If you are not motivated enough to stage this uncomfortable intervention, I assure you he won’t be motivated to go. This is the kind of thing a psychiatrist should be telling you, not trying to sell you on Suboxone.  Nobody likes confrontation or to be confronted. Ten people.  Minimum.  Sure, you are partly guilting them into treatment, partly coercing.  But getting them into treatment in this way is better than not getting them into treatment in a nicer way.  Psychiatry is war.
Sometimes people don’t need to know.  If a person’s life is changed on medication, it may be okay not to tell them all the side effects.  I know, lawyers are standing by (see # (blame lawyers),  but again, it’s strategy, and I think reasonable people (i.e. juries) will understand what you were doing.  If lithium keeps the person from slitting their own throat, it’s okay to skip the part about how it can hurt your thyroid.  It doesn’t exempt the doctor from checking for it, mind you.  In these tricky situations, a) you have to be sure this medication is absolutely vital; b) recruit as many people as possible into the therapeutic umbrella.  Tell the wife about the side effect; tell family what to watch out for.  And monitor.  There’s even a technical term for this therapeutic privilege, but I can’t remember what it was.
Save the environment.  Here’s an all too common scenario involving no strategic thinking:  Your adult child is living at home, no job, sporadic drug use, involved in an abusive relationship, frequent quasi-suicidal acts, etc. You’ve tried everything, nothing has worked.  You don’t know what to do. You’re afraid to kick them out because  they can’t manage on their own, you’re afraid they’d sink deeper into drugs/depression/etc;  but on the other hand you have other kids you have to worry about, a finite supply of money, etc, etc. You’re paralyzed.

Here’s a question you might not have thought about: what happens to the kid when you die? They are suddenly going to be without support, suddenly without money, suddenly without resources.  Will they simply manipulate your spouse into getting their needs met?  Or worse, go somewhere else? Is that what you want?  Plan today, now, for this eventuality.  Maybe that means setting up a trust with a finite monthly payout only if they are living on their own and have a paycheck.  Or only if they are seeing a therapist once a week.  Or give clean urines.  “What is this, probation?”  Actually, that’s exactly what it is.

You have to save the environment you are in before you can help the other person.  That means protecting your wife and other kids, and their physical assets. It means protecting your marriage.   It may seem cold to worry about money when your kid’s on heroin, but I assure you that this is the most important thing you can do if the kid won’t get help.  Ripping apart your marriage over this benefits no one, absolutely no one. So yes, it may mean kicking them out of the house, cutting them off.  It also means doing an intervention.  It means holding your breath that that phone is going to ring in the middle of the night and it’s going to be the police.  But letting them eat, sleep, and watch TV in your house while their chaos continues does not lessen the risk of receiving that phone call.

It’s called enabling.  Don’t do it.  And a psychiatrist should be telling you this, not trying to give you Celexa to help you cope with it.

8. Polypharmacy

Polypharmacy isn’t just common– it’s the codified standard.  When two psychiatrists discuss a patient, inevitably one of them will say these four words: “You should consider adding…”

The paradigm is that if you fail a medication, you must be so sick that you need a second medication.

It’s a useful paradigm; and by useful, of course, I mean wrong.  Here’s an alternative paradigm: maybe if the medication didn’t work, you should try a different one?

Polypharmacy would be ok if there was at least some data justifying it.  But there isn’t.  I know, controversial.  Look it up.

Consider antipsychotics: if anyone can provide the logic– not data, simply the logic– for using two simultaneously, I’d love to hear it.  Antipsychotics work by blocking dopamine receptors, of which there are supposedly a finite number.  If one antipsychotic blocks most of them, where is the other supposed to go?  Why couldn’t you simply increase the dose of the first? And if side effects prevent this increase, why wouldn’t you just switch to the second medication?

Same with antidepressants: Zoloft and Prozac are SSRIs, they target the exact same molecule, which is again finite in number.  If most are blocked by one drug, where does the second go?  Why are you offended that Medicaid doesn’t let you prescribe two at the same time?

So you say: well, what about mixing two drugs of differing pharmacologies, like Zoloft (serotonin) and Wellbutrin (dopamine/norepinephrine)?  At least there is logic to this one, but–surprise- no evidence.  It may seem as though Zoloft + Wellbutrin, or Depakote + an antipsychotic, etc is better than one alone, but they’re not.    But here’s the point: even if it were true, so what?  How do you know it’s necessary?  Shouldn’t prudence and common sense and fiscal responsibility and the cramp in your writing hand require you to at least try monotherapy a few times?  Twice, at least? Because I can’t prove two drugs are better than one, but I can prove they are twice as toxic and twice as expensive.

Polypharmacy is bastard child of the theory of maintenance treatment.  If it took three medications to get you feeling better, then you need to continue these three medications in order to stay stable.  Going off your medications results in disaster.

First of all, no.  Secondly, take the example of mania.  If you’re manic, and it took three medications to bring the mania down, does that mean you need those three for the rest of your life?  Because if so, what do you do the next time you get manic?  Add a fourth?  Don’t you get used to medications?  Does tolerance not occur?  Upregulation and all that? You see the problem– maintenance begats polypharmacy.  Also, medications have side effects, and so medications are given for the side effects of the other

medications, ad nauseum.  At some point (four medications?) the symptoms you are seeing cannot be reliably ascribed to the disorder rather than the medications themselves.  The patient is buried.  The treatment now becomes getting them off these medications.

Again: it may be true that an individual person needs several medications. But you can’t make polypharmacy a generalized treatment standard.  It’s too expensive and has too many side effects for a theoretical benefit.  And what kind of message does it send to the patient?    If you’re on four medications, how can you be anything but severely ill, all the time?  How can you be responsible for any of your feelings, or for controlling them?

 

9. Diagnose everything

The layman’s argument is that psychiatry pathologizes everything:  “well, anyone would be depressed in those circumstances.  How is that an illness? And why can you get SSI for it?”

But the truth is in the nuances.  When psychiatrists ask you to keep a mood chart, and you report that on these two days your “depression was worse,” what allows the psychiatrist to know that wasn’t normal sadness? Can a bipolar ever be sad for a month and not be depressed?

If a person beats his girlfriends, kills cats, and gets brought by the police because he set fire to a rival’s car, is it possible that his Axis I diagnosis is—nothing?  Ok—how many times have you actually written that down?  How many times have you terminated the “treatment,” or refused to uphold an involuntary commitment order, because the case was not psychiatric?  I know, the system does not have a good mechanism for doing this.  I feel your pain.  But every time we give some vague “Not Otherwise Specified” diagnosis or pass them along to the inpatient services, we are creating a social policy disaster.  We are confirming to the laymen that we think these behaviors are psychiatric, that they are rightfully our purview,  and ensuring that a) we will be held responsible for dealing with them; b) we will be held responsible for the outcome.

Thanks for installing the Bottom of every post plugin by Corey Salzano. Contact me if you need custom WordPress plugins or website design.

Psychological Defenses

Defense mechanisms are automatic psychological processes that protect an individual from anxiety and the awareness of internal or external threats or stressors. People are often unaware of these processes as they operate (although others may be painfully aware of them!). Defense mechanisms can be classified into groups or levels that indicate how they affect an individual’s functioning.

High Adaptive Level: Defense mechanisms in this group result in optimal adaptation to stress. The defenses usually maximize feelings of well being and do not interfere with the conscious awareness of feelings, ideas, and their consequences.

•Affiliation involves dealing with stressors by turning to others for help or support. This involves sharing problems with others but not trying to make someone else responsible for them.

•Altruism involves dealing with stressors by dedicating yourself to meeting the needs of others. The individual receives satisfaction vicariously or from the response of others.

•Anticipation involves dealing with stressors by anticipating the consequences and feelings associated with possible future events and considering realistic solutions.

•Humor involves dealing with stress by emphasizing the amusing or ironic aspects of the situation.

•Self-Assertion involves dealing with stress by expressing your feelings and thoughts directly in a way that is not aggressive, coercive, or manipulative.

•Self-Observation involves dealing with stress by reflecting on your own thoughts, feelings, motivation, and behavior, and then responding appropriately.

•Sublimation involves dealing with stress by channeling potentially disruptive feelings or impulses into socially acceptable behavior (e.g., playing rugby to channel angry impulses).

•Suppression involves dealing with stress by intentionally avoiding thinking about disturbing problems, wishes, feelings, or experiences.

Mental Inhibition Level: Defense mechanisms in this group keep potentially threatening ideas, feelings, memories, wishes, or fears out of awareness. Diminished awareness can affect the person’s ability to relate to others.

•Displacement involves dealing with stress by transferring strong feelings about on situation onto another (usually less threatening) substitute situation.

•Dissociation involves dealing with stress by breaking off part of memory, consciousness, or perception of self or the environment to avoid a problem situation (e.g., amnesia).

•Intellectualization involves dealing with stress by excessively using abstract thinking and generalizations to avoid or minimize unpleasant feelings.

•Reaction Formation involves dealing with stress by substituting behavior, thoughts, or feelings that are the exact opposite of your own unacceptable thoughts or feelings (which the person is usually not aware of).

•Repression involves dealing with stress by removing disturbing wishes, thoughts, or experiences from conscious awareness. The person may still be aware of the feelings associated with the repressed issue, but will not know where the feelings come from.

•Undoing involves dealing with stress by using words or behaviors designed to negate or make amends symbolically for unacceptable thoughts, feelings, or actions.

Disavowal Level: Defense mechanisms in this category try to keep unpleasant or unacceptable stressors, impulses, ideas, feelings, or responsibilities out of awareness.

•Denial involves dealing with stress by refusing to acknowledge some painful aspect of reality or experience that is apparent to others.

•Projection involves dealing with stress by falsely attributing your own unacceptable feelings, impulses, or thoughts to another person.

•Rationalization involves dealing with stress by concealing the true motivations for a thought, action, or feeling by using elaborate, reassuring, and self-serving (but incorrect) explanations.

Action Level: This level is characterized by defenses that deal with internal or external stressors by action or withdrawal.

•Acting Out involves dealing with stress by using action rather than reflection or feeling. Defensive acting out is often associated with “bad behavior” when there are underlying emotional conflicts.

•Help-Rejecting Complaining involves dealing with stress by complaining and making repeated requests for help that disguise hidden feelings of hostility toward others, which is then expressed by rejecting the suggestions, advice, or help that others offer. The complaints may involve physical or psychological symptoms or life problems.

•Passive Aggression involves dealing with stress by indirectly and unassertively expressing aggression toward others. The person displays an outward superficial cooperativeness that masks the underlying resistance, resentment, and hostility. This defense may be adaptive in situations where direct and assertive communication is punished (e.g., abusive relationships).

Thanks for installing the Bottom of every post plugin by Corey Salzano. Contact me if you need custom WordPress plugins or website design.

Neuroanatomical, Neurophysiological and Neuropsychological Terminology

This table lists the original Greek and Latin meanings of neuroscience words. Most of the words are neuroanatomical terms, but neurological symptoms and disorders are also included.

WORD           MEANING

abducens…..drawing away
ablation…..carrying away
acetylcholine…..vinegar bile
adrenalin…..near the kidney
afferent…..to carry
agnosia…..no knowledge
alar…..wing-like
alexia…..no words
alveus…..canal
amacrine…..no long fiber
ambidextrous…..both right
ambiguus…..doubtful
amblyopia…..dull vision
amnesia…..forgetfulness
ampulla…..small bottle
amygdala…..almond
analgesia…..no pain
aneurysm…..widening
anesthesia…..no sensation
ansa…..urn handle
antitoxin…..against poison
aphagia…..no eat
aphasia…..no speech
aqueduct…..water canal
arachnoid…..spider web-like
arbor vitae…..tree of life
arcuate n……bow shaped
astigmatism…..not a point
astrocyte…..star-like cell
ataxia…..not orderly
atrophy…..want of nourishment
auditory…..to hear
aura…..breath, breeze
auricle…..a little ear
autonomic…..self law
axon…..axis, axle
basilar…..base
bouton…..button
brachium…..arm
bregma…..front of the head
calcarine…..spur-shaped
callosum…..hard, tough
cannula…..reed
carotid…..to put to sleep
cataplexy…..down stroke, seizure
catatonia…..down tone
cauda…..tail
cauda equina…..horse tail
caudate…..tail
causalgia…..burning pain
cenereum…..ash gray
cephalic…..head
cerebellum…..little brain
cerebrum…..brain
ceruleus…..blue
cerumen…..wax
cervical…..neck
chiasm…..a crossing
chorea…..to dance
choroid…..like a membrane
ciliary…..eyelash
cinereum…..ashen-hued
cingulum…..girdle or belt
circadian…..about a day
cistern…..reservior or well
claustrum…..barrier
coccyx…..cuckoo
cochlea…..snail shell
colliculus…..little hill
conscious…..aware
conus…..cone or peg
coma…..deep sleep
commissure…..joining together
conjunctivum…..join
convolution…..a turn, a folding
convulsion…..pulling together
cornu…..horn
corona…..crown
corpus…..body
cortex…..bark, shell, outer layer
cribiform…..sieve-like
crista…..crest
cruciate…..cross-shaped
crus…..leg
culmen…..ridge, summit
cuneate…..wedge
cupula…..little tub
decussation…..crossing
dementia…..away from mind
dendrite…..tree
dentate…..notched
dura…..hard
dyskinesia…..improper motion
edema…..swelling
efferent….carry out (away)
emboliform…..plug-like
encephalitis…..brain inflammation
encephalogram…..brain writing
ependyma…..upper garment
epilepsy…..seizure
ethmoid…..sieve-like
falx…..sickle
fasciculus…..little bundle
femoral…..thigh
filum…..thread
fimbria…..fringe
fissure…..cleft or slit
flocculus…..tuft of wool
folium…..leaf
foramen…..opening
fornix…..arch
fossa…..trench, channel
fovea…..pit, depression
fundus…..bottom
funiculus…..little cord
fusiform…..spindle-shaped
ganglion…..knot, swelling
genu…..knee
geniculate…..bent like a knee
glabrous…..bald
gland…..acorn
glia…..glue
globus pallidus…..pale ball
glossal…..tongue
gracile…..slender
gyrus…..ring, circle
habenula…..rein
hallucination…..to wander in the mind
hemorrhage…..to burst forth with blood
hippocampus…..sea horse
hypnosis…..sleep
hypoglossal…..under the tongue
hypophysis…..down growth
hypothalamus….under thalamus
incus…..anvil
infundibulum…..funnel
insula…..island
iris…..rainbow
lamina…..layer, thin plate
lemniscus…..woolen band or filet
lens…..lentil
lenticular…..shaped like a lens
limbic…..border, hem, fringe
lingula…..little tongue
lumbar…..pertaining to the loins
macula…..spot
malleus…..hammer
mater (dura)…..mother
medulla…..innermost, marrow
melanin…..black
meninges…..membrane
meningitis…..membrane inflammation
microglia…..small glue
myelin…..marrow
myopia…..to shut eye
narcolepsy…..numbness seizure
narcotic…..benumbing, deadening
neuron…..nerve
node…..knot
nucleus…..nut
obex…..barrier
oblongata…..rather long
oculomotor…..eye movement
oligodendrocyte…..few tree cell
operculus…..cover, lid
optic…..for sight
oscilloscope…..to examine swinging
pallidus…..pale
paralysis…..to loosen
paranoia…..mind beside itself
parietal…..wall
patella…..little plate
peduncle…..stemlike
pellucidum…..translucent
pia…..soft
pineal…..pine cone
pinna….wing
piriform…..pear-shaped
pituitary…..slime, mucous
placebo…..to please
plexus…..a braid
pons…..bridge
potential…..power
pterygoid…..wing-shaped
pulp…..flesh
pulvinar…..cushion, pillow, couch
pupil…..doll, little girl
putamen…..shell
pyramis…..pyramid
pyriform…..pear-shaped
quadrigemina…..four twins
rabies…..to rage
ramus…..branch
raphe…..seam
rectus…..straight
restiform…..rope-like
reticular…..net-like
rhodopsin…..rose eye
rostral…..beak
rubro…..red
sacral…..sacred, holy
sagittal…..arrow
schizophrenia…..split mind
sclera…..hard
sella turcica…..Turkish saddle
semilunar…..half moon
serotonin…..blood stretching
septum…..wall, partition
sinus…..a hollow
soma…..body
somnambulism…..sleep walk
somniloquism…..sleep speak (talk)
spine…..thorn
splenium…..bandage
stapes…..stirrup
stellate…..star
stimulate…..to goad
striated…..striped
substantia nigra…..black substance
sulcus…..groove, trench, furrow
synapse…..connection
synesthesia…..together perception
tapetum…..carpet
tectum…..roof
tegmentum…..covering
temporal…..time
tentorium…..tent
thalamus…..inner chamber
thoracic…..chest
trabecula…..little beam
tremor….to shake
trigeminal…..three twins
trochlear…..pulley
tubercle…..swelling
uncus…..hook
vagus…..wandering
velum…..covering
ventricle…..small cavity
vermis…..worm
vertex…..top, summit
vesicle…..blister, bladder
vitreous…..glassy

Thanks for installing the Bottom of every post plugin by Corey Salzano. Contact me if you need custom WordPress plugins or website design.

New medications for Adults with Attention Deficit Disorder

It has long appeared that the medication situation for AD/HD was reversed from that of other psychiatric conditions. For other conditions, psychiatrists who treated children and adolescents had relatively fewer medications that had actually been tested on children. We had to extrapolate from adult data, make do with fewer medications, and base our prescribing practices on less research data. Child psychopharmacology seemed like the stepchild of adult psychopharmacology. The exception was AD/HD. This was the condition child psychiatrists could call their own. Although medication choices were still more limited than they are today, clinicians still had more information on how the medications affected AD/HD children than they did on how the same medications affected adults. The tables were turned. The adults were the ones with less data and fewer medication options. It used to be quite controversial to give stimulant medication to older adolescents, let alone adults. However, some adults did get stimulant medication for AD/HD. Usually it involved adolescents who simply continued treatmrnt after they turned 18. Second opinions or special permission from the Drug Enforcement Agency were necessary if one wanted to prescribe stimulants to an adult with AD/HD. Tricyclic antidepressants could be a less controversial choice.

Over the past 10-15 years, it has become easier and less controversial to diagnose and treat adult AD/HD. Medication options have expanded, but stimulant medications, usually methylphenidate (Ritalin) and dextroamphetamine compounds (Dextrostat, Dexedrine Spansules and Adderall) are still a frequent starting place in the pharmacological treatment of AD/HD.

Adults and children may have different medical considerations:

Although there is still more information on pediatric AD/HD, there is an emerging body of knowledge specific to medication for adult AD/HD. Many of the medications are the same as those used for children and adolescents. However, when treating adults, there are several general differences to consider. Although adults are generally larger, their liver and kidney function may not be as robust as children. Thus an adult may need less of a particular medication per pound of body weight. A given dose of medication may hang around longer in the adult’s system.

Adults are more likely to be taking medications for other medical conditions such as high blood pressure or diabetes. These may interact with the AD/HD medication. Conversely, some of these other medications may cause inattention and thus exacerbate or mimic AD/HD. For example, a clinician from another state referred me a patient with possible AD/HD. It turned out that an anxiety disorder, along with two medications she was taking, caused her inattention.

Polypharmacy, (prescribing several psychiatric medications at the same time) has become more common. Adult AD/HD by itself often requires more than one medication to control all of the AD/HD symptoms. If the individual has another disorder, such as depression, one may need to medicate this too. I have mixed feelings about the trend towards polypharmacy. When done carefully and systematically, it can bring relief to individuals who have experienced distressing symptoms. However, if done in a rapid or cavalier fashion, it can lead to medical side effects, or it can exacerbate the very symptoms it was meant to treat.

The stimulants, including methylphenidate (Ritalin) and amphetamine (Dexedrine and others) along with some tricyclics (such as Desipramine), have demonstrated efficacy in the treatment of adult and childhood AD/HD. The stimulants have a 60 to 80% response rate. However, some individuals respond partially or not at all. Others develop uncomfortable side effects. Atomoxetine (see below) is a non-stimulant medication approved for the treatment of AD/HD Currently we have several second-line medications (not FDA approved for AD/HD), but we need more medication choices. We also need more high-quality research, particularly in how adults with AD/HD respond to pharmacological treatment. The following is a brief overview of some of the emerging developments in the field.

Current Second and Third-Line Medications: Alpha agonists, bupropion, (Wellbutrin) and the tricyclic antidepressants. Other medications often used for comorbid disorders or ADHD-related symptoms: SSRIs (eg. Prozac, Zoloft and others) mood stabilizers (Lithium, Depakote, Tegretol) and the atypical antipsychotics.

Longer Duration Stimulant Medications

Slow Release Methylphenidate

Methylphenidate (Ritalin) is a short-acting drug. It can be difficult to remember several doses per day.

Ritalin SR, one of the older slow-release stimulants, often seems to show inconsistent results. It comes in 20mg pills and cannot be split into smaller fragments. The duration of effects may not always be consistent. Metadate-ER manufactured by Celltech, was released in 10mg and 20mg sizes. Metadate-ER is similar to Ritalin-SR. The active component, methylphenidate, is in a wax-like matrix that releases the drug over time. It lasts about 4-8 hours.

Metadate CD: Released by Celltech in 2001, uses a delivery system called Diffucaps. more recently released which uses a different delivery system. Its peak effect is generally around 5 hours and its effect lasts 8 hours. Metadate CD capsules contain two types of beads. About 30% of the medication is released immediately. The remainder is released over time through beads with a release-control membrane. If the individual cannot swallow the capsule, one can open the capsule and sprinkle the beads on food. The medication has a first peak at about 1.5 hours and a second, larger peak at about 4.5 hours after ingestion.

Ritalin LA: Released in 2002 by Novartis (the makers of brand name Ritalin)  this medication is a capsule in which 50% of the beads release the methylphenidate immediately and 50% are released abour four hours later. As compared to Concerta and Metadate CD, this medication gives a stronger earlier dose and relatively less medication in the afternoon. the duration of efficacy is about 6-8 hours.

Concerta  (McNeil Pharmaceuticals) is a form of Methylphenidate that uses an osmotic system to deliver methylphenidate in a pulsed pattern. This allows a 12 hour response from a single daily dose. It may prove to be more reliable than Ritalin-SR. Concerta was released in August 2000. The osmotic “oros” system has been used successfully for several years for a diabetes medication and a bladder control medication. With Concerta, the methylphenidate level does not rise as fast as it would with Metadate CD, but the Concerta lasts longer than Metadate CD or Ritalin SR. Drug studies suggest that its duration of action is 12 hours, but I have seen a number of patients who seem to get a shorter duration of effect at all dosage levels.

Focalin and Focalin XR: Novartis, the manufacturer of brand name Ritalin, has released a non-racemic form of methylphenidate. Other forms of methylphenidate such as Concerta and Metadate are mixtures of two mirror images (isomers) of the methylphenidate molecule. The body may metabolize the dextro (right handed) form of a compound differently from its mirror image the levo (left handed) form.  In the case of methylphenidate, the dextro isomer is the active componentactive and the levo isomer  you switch from regular methylphenidate to Focalin, you start with half as much Focalin.

Daytrana: Shire released a skin patch form of methylphenidate. The FDA has only approved its use in children aged 6-12. It’s commercial release was delayed because of FDA safety concerns but after extended testing was done the FDA gave its approval. There are some theoretical concerns about skin sensitization. I would recommend that adults defer using this medication until there is further testing in other age groups. For more information on this medication, see our article on Daytrana.

Slow Release amphetamines:

Dexedrine Spansules, a long-acting form of d-amphetamine, has been on the market for years. It has a peak effect in 1-4 hours and lasts 6-10 hours. It tends to have a more gradual tapering and thus may have less of a rebound effect. Adderall is a mixture of four salts of d-amphetamine combined with a smaller amount of the less active r-amphetamine. Some clinicians felt that Adderall had a longer duration of action than regular d-amphetamine. However, there are as of yet, no published studies showing that it lasts any longer than short-acting d-amphetamine. Thus we cannot really classify regular Adderall as a long-acting stimulant.

Adderall XR: In 2001, Shire, the manufacturer of Adderall, released Adderall XR. In this formulation, the Adderall is encapsulated in coated beads inside of a capsule. Half of the beads dissolve immediately, and the other half dissolve about 4-6 hours later. There are, as yet, no published studies comparing Adderall XR to the less expensive Dexedrine Spansules. However some patients appear to do better on Adderall XR with its d and r-dextroamphetamine combination. Others do better on Dexedrine Spansules–the all d-amphetamine compound. 

SPD465 Shire Pharmaceuticals is working an a compound with the same active ingredient as Adderall (mixed salts amphetamine) which will last 16 hours. It will be marketed for adults and children.

NRP104 New River Pharmaceuticals is developing a medication which would be marketed by Shire Pharmaceuticals. (lisdexamfetamine dimesylate) D-Amphetamine is bonded to l-lyseine, an amino acid. The drug is not active until it is converted into d-amphetamine in the body. Early results suggest that ti has a lower abuse liability than do the other amphetamines. The peak effect is later than that of regular d-amphetamine and it appears less likely to cause euphoria.

Generic methylphenidate or d-amphetamine are fairly inexpensive. However, many of the longer acting stimulants can be quite expensive for those without a good pharmacy plan.

Non Stimulant Medications

Atomoxetine   (Strattera, from Lilly Pharmaceuticals), was approved by the FDA for distribution in November 2002. It became available in US pharmacies in early 2003. Despite its hefty price tag, it is becoming widely used for adults and children with Attention Deficit Hyperactivity Disorder. (AD/HD) It is a non-stimulant medication approved for the treatment of AD/HD in both children and adults. It was the first medication that the FDA specifically approved for the treatment of ADHD in adults. Atomoxetine is a selective norepinephrine reuptake inhibitor. This means that it strengthens the chemical signal between those nerves that use norepinephrine to send messages. Atomoxetine does not appear to affect the dopamine systems as directly as do the stimulants.   It is often prescribed once per day, but those who have trouble with gastrointestinal upset, can take a smaller dose twice a day. Common side effects are headache, abdominal pain, nausea, vomiting, weight loss anxiety, sleepiness and insomnia. It can also interfere with sexual performance in adults. It appeared to cause less insomnia and appetite suppression than methylphenidate. However it may cause a higher incidence of sleepiness and vomiting than methylphenidate. It is most commonly administered once a day. The clinical effect appears to last all day and even into the next morning. I sometimes prescribe it twice a day to minimize the nausea. It can be quite helpful to those who cannot tolerate stimulants. However, some patients say that it does not give as strong an effect as what they get from the stimulants. See our expanded article onAtomoxetine

Modafinil (Provigil) has been approved for treatment of narcolepsy in adults. It is chemically unrelated to methylphenidate or amphetamine. When compared to methylphenidate and amphetamine, it seems less likely to cause irritability and jitteriness. It appears to act on the frontal cortex and is more selective in its area of action than the traditional stimulants. Cephalon  In studies of adults with ADHD, there was a small, promising study suggesting that it might be effective for adults with ADHD. However a larger study sponsored by Cephalon indicated that Modafinil was no more effective than placebo. Some of their studies suggested a positive effect on children when larger doses are used. In the summer of 2006, the FDA announced that it would not approve Modafinil for children with AD/HD. The FDA felt that the medicaiton did not show significant advantages over existing ADHD medications, and expressed concern about side effects in the higher doses necessary to effectively treat AD/HD.

Bupropion SR and XL (Wellbutrin) has been used to treat AD/HD for several years. A recent controlled study showed that it is effective in the treatment of AD/HD symptoms in adults. Its structure is chemically similar to amphetamine, but does not have the same abuse potential. It should not be used in individuals with bulimia or a seizure disorder. In my experience, it is not as powerful as the stimulants, but is useful for individuals who cannot tolerate stimulants or for whom a Schedule II drug is inadvisable.

Alpha-2A-adrenoceptor agonist:   Clonidine (Catapress) and guanfacine (Tenex) have been used in adults for the contol of high blood pressure. However, they are also useful in AD/HD, particularly for those with tics, impulsivity or aggression. Like clonidine, guanfacine can reduce tics for individuals with Tourette Syndrome. Because of its sedating properties, clonidine is sometimes used to help people with ADHD fall asleep. Since both clonidine and guanfacine can affect blood pressure and heart rate, it is a good idea to monitor blood pressure and get an EKG to check the heart rhythm. There have been a few reports of sudden death in children associated with the stimulant/clonidine combination, but some researchers have questioned whether some of those deaths were truly related to the medication.   Because cuanfacine lasts longer than clonidine, only one or two doses are needed each day. Recent research confirmed that it can be useful in children, especially the 30% who have difficulty tolerating stimulants. These medications can help all of the symptoms of AD/HD but often seem to help impulsivity motor hyperactivity and irritability more than attention. In some cases, clonidine or guanfacine is combined with a stimulant if the stimulant does not have enough effect on irritability and impulsivity. Shire Pharmaceuticals is working on a long-acting form of guanfacine (Connexyn) which it will market as a non-stimulant drug for ADHD for children aged 6-17 years.

Selegiline (Eldepryl)  is a monoamine oxidase inhibitor used to treat symptoms of Parkinson’s Disease. If one uses low doses, it may not be necessary to follow the restrictive diet associated with its cousins, the antidepressants Parnate and Nardil. A small controlled study showed that children with severe AD/HD and co-morbid conditions, demonstrated improvement in learning and classroom behavior on 5 mg twice a day. However there have been mixed results in adults with AD/HD.

Effexor and Effexor-XR (venlafaxine) An open trial (not a controlled study) with adults suggested that it might be helpful for some adults with AD/HD. In an open, 5-week study of children and adolescents with AD/HD, some individuals showed an improvement in behavioral but not cognitive measures. Several experienced worsening of their AD/HD symptoms and 25% could not tolerate the medication due to side effects. It is a good idea to monitor blood pressure since some individuals on Effexor show a rise in blood pressure. Sudden discontinuation of Effexor may lead to nausea and vomiting.

Mood Stabilizers are traditionally used for Bipolar Disorder. (Manic Depressive Disorder) These medications include Lithium and several anticonvulsant (seizure) medications such as Depakote (valproate) Tegretol (carbamazepine) and others. There is debate among psychiatrists about the percentage of AD/HD individuals who also have Bipolar Disorder. Some see the mood swings as part of the AD/HD. Others see it as a sign of a separate, co-existing disorder. In either case, the mood stabilizers may be useful to help modulate irritability and rapid mood shifts. These medications require closer medical monitoring. Blood tests and sometimes an EKG may be required. If an adult appears to have both AD/HD and Bipolar Disorder, one often treats the Bipolar Disorder first and then treats the AD/HD. Individuals with both conditions have a significantly increased incidence of substance abuse. Since illegal drugs can have dangerous interactions with some prescribed medications, drug screens may be advisable.

Estrogen Supplementation Some women report that their AD/HD symptoms worsen in the premenstrual period and during the peri-menopausal years. Low or fluctuating levels of estrogen might lead to depressed mood or a worsening of one’s ADHD. Some women with and without AD/HD have reported improvement in memory and attention span after estrogen supplementation. A women who has hormone-related exacerbation of mood or attention span might benefit from a stimulant, estrogen supplementation, an SSRI or a combination of these medications. Since estrogen affects many systems in the body, each woman should review the risks and benefits with her gynecologist. More systematic research is needed. (See Pat Quinn’s article in Nov/Dec 2000 Attention Magazine. Recent data reported in this spring in JAMA from the WHMS study suggested that estrogen-progesterone supplementation might actually accelerate the progress of memory impairment and dementia in postmenopausal women. Information on the effect of estrogen alone (on women with hysterectomies) has not yet been released.

Nicotinic Analogues (Medications that act on some of the same brain receptors as nicotine.) Much of the work on the neurological basis for AD/HD has focused on the regulation of dopamine and noradrenergic neurotransmitters. However, there has been a suggestion that poor regulation of the nicotinic receptors may also be involved. Nicotine enhances dopaminergic neurotransmission. Individuals with AD/HD have an increased rate of cigarette smoking. A small study suggested that a transdermal nicotine patch improved AD/HD symptoms in ADHD adults. Studies may focus on more selective compounds in this category that produce an effect without the negative side effects of nicotine. (selective cholinergic channel activators.)

Pemoline (Cylert) The FDA has recommended that individuals who are still taking this medication be switched over to other treatments. This revised recommendation was made in response to several reported cases of liver failure.

Stimulant Medications: Duration of Action

Medication Frequency Peak Effect Duration of Action
Dexedrine (d-amphetamine) 2 or 3 times per day 1-3 hours 5 hours
Adderall 2 or 3 times per day 1-3 hours 5 hours
Dexedrine Spansules Once in am 1-4 hours 6-9 hours
Adderall XR Once in am 1-4 hours 9 hours
Ritalin 3 times per day 1-3 hours 2-4 hours
Focalin 2 times per day 1-4 hours 2-5 hours
Ritalin SR 1 or 2 times a day 3 hours 5 hours
Metadate CD Once in am 5 hours 8 hours
Concerta Once in am 8 hours 12 hours

 

 

Adderall and prescription ADHD medications can be highly dangerous if abused. These stimulants have many adverse side effects and are known to be quite harmful to children despite being FDA approved.

Since Adderall abuse has grown to epidemic levels, cogni research team has compiled an article about the best all-natural alternatives to Adderall (Updated for 2018).Read more on CogniTunes.

 

12 Best Adderall Alternatives: Natural Over the Counter ADHD Substitutes

Thanks for installing the Bottom of every post plugin by Corey Salzano. Contact me if you need custom WordPress plugins or website design.

Malaria vaccines could make the disease worse

Malaria vaccines could make malaria nastier. In mice given an experimental vaccine now in trials, the malaria parasite evolved to get round the immunity – and in the process caused more severe disease.

Malaria kills 2000 children every day, sickens millions repeatedly, and helps keep tropical nations in poverty. Yet there is still no vaccine, partly because the parasite takes different forms as it moves from mosquitoes to human blood, to liver cells, red blood cells and back to mosquitoes.

One malaria vaccine – RTS,S – is in large-scale trials. It targets the liver stage of the parasite. Other vaccines in trials target the blood-cell stage, and contain a parasite protein called AMA-1, meant to prime the body’s immune system to attack it.

These vaccines all seem likely to be “leaky”, allowing vaccinated people to still acquire and transmit some parasites. Parasites that pass through vaccinated people this way could start resisting the vaccine in two ways, saysAndrew Read at Pennsylvania State University in University Park. The parasites’ AMA-1 could change so that vaccine-induced immunity won’t recognise it, a process called immune escape. Or parasites may emerge that dodge immunity in other ways, which could make the disease more virulent.

Rise in virulence

In 2004 Read tested this by passing mouse malaria repeatedly between mice made immune by natural infection. Those parasites indeed became more virulent, but it wasn’t clear how.

Read has now repeated the experiment using an AMA-1 vaccine. His team passed blood-cell-stage malaria parasites 10 times between mice that had been given the AMA-1 vaccine. By the end, the parasites reached higher densities, and caused more anaemia, than those passed between unvaccinated mice. Parasites from vaccinated mice were more virulent in unvaccinated mice as well.

“The real eye-opener was that there was no immune escape,” says Read. “Parasite AMA-1 was unchanged.”

Boosted deadliness

Instead, the parasites had other changes in gene activity that allowed them to escape vaccine-induced immunity, and these changes also made them more virulent. A vaccine that did this in people would lose its effectiveness very quickly, says Read, while boosting the deadliness of local malaria, particularly for unvaccinated people.

Clinical trials test whether vaccines protect people from disease, but don’t look for impacts on the actual pathogens, apart from some that have tracked immune escape. Read says that in future such trials should also track which genes are active in malaria parasites in vaccinated people.

Chris Plowe at the University of Maryland in Baltimore, who works on AMA-1 vaccines, agrees. It could be difficult, however, as agencies that fund vaccine trials do not normally fund such tracking.

Journal reference: PLoS Biology, DOI: 10.1371/journal.pbio.1001368

Thanks for installing the Bottom of every post plugin by Corey Salzano. Contact me if you need custom WordPress plugins or website design.

Hot, Hot, HOT!-Can spicy food actually make you lose weight? Dev Goswami finds out…

When there are issues as big as weight loss there are bound to be loads of fads and diets that claim to help you lose that extra weight, each promising to be more effective than the other. The effect of this is that half truths sometimes become the complete truth to the extent that people start saying you will not lose weight if you do not do this.

One such half truth is that spicy food will make you lose weight. This is not completely false but not completely true either. Sheru Aangarish, an international health and fitness expert, says, “Spicy food will only help you lose weight up to a certain extent. I would never advise relying only on spicy food to burn off excess fat because it is responsible for other health problems — ulcers and high blood pressure are the two most common problems caused due to spicy food.”

Spicy food does play a role in boosting your metabolism and the faster the metabolism, greater is the weight loss. Sheru adds, “The main compound responsible for losing weight with respect to spicy food is chromium picolinate (found in black pepper). It’s a natural burner which raises our body temperature and this results in the fat burning process taking place.”

Also, spicy food is known to make people eat less, thus reducing their overall calorie consumption which is the actual reason behind the weight loss. It is very important to keep this fact in mind because it is rarely mentioned that spicy food will help boost metabolism and decrease appetite.

Apart from the adverse health effects mentioned above, a surplus intake of spicy food is also responsible for the following health problems:
• It can result in infections in the stomach resulting in inflammation of the stomach lining leading to gastritis.

• Burping after a spicy meal is not just bad manners but the body’s inability to deal with spicy food. The acid reflux caused by spicy food can cause your teeth to erode.

• It is said that after a period of time the tongue gets used to the spiciness and thus you stop getting the taste. But what actually happens is that your sense of taste gets deteriorated if you constantly eat spicy food.

While there is no denying the positive impacts spicy food can have on your body, the negative impacts shouldn’t be discounted. However, you do not have to lose sleep over spicy food. Just remember to keep it in check and not go overboard. With respect to weight loss you can still have spicy food to help you. Sheru says, “One thing I can recommend is black pepper balls which, due the chromium picolinate content, is backed up by research that claims it will help you lose weight.”

Thanks for installing the Bottom of every post plugin by Corey Salzano. Contact me if you need custom WordPress plugins or website design.

Advice from Somewhere

ONE.Give people more than they expect and do it cheerfully.

 

TWO.Marry a man/woman you love to talk to. As you get older, their conversational skills will be as important as any other.

 

THREE.Don’t believe all you hear, spend all you have or sleep all you want.

 

FOUR.When you say, “I love you,” mean it.

 

FIVE.When you say, “I’m sorry,” look the person in the eye.

 

SIX.Be engaged at least six months before you get married.

 

SEVEN.Believe in love at first sight.

 

EIGHT.Never laugh at anyone’s dreams. People who don’t have dreams don’t have much.

 

NINE.Love deeply and passionately. You might get hurt but it’s the only way to live life completely.

 

TEN.In disagreements, fight fairly. Please No name calling.

 

ELEVEN.Don’t judge people by their relatives.

 

TWELVE.Talk slowly but think quickly.

 

THIRTEEN.When someone asks you a question you don’t want to answer, smile and ask, “Why do you want to know?”

 

FOURTEEN.Remember that great love and great achievements involve great risk.

 

FIFTEEN.Say “bless you” when you hear someone sneeze.

 

SIXTEEN.When you lose, don’t lose the lesson.

 

SEVENTEEN.Remember the three R’s:
Respect for self;
Respect for others;
Responsibility for all your actions.

 

EIGHTEEN.Don’t let a little dispute injure a great friendship.

 

NINETEEN.When you realize you’ve made a mistake, take immediate steps to correct it.

 

TWENTY.Smile when picking up the phone. The caller will hear it in your voice.

 

TWENTY-ONE.Spend some time alone.

Thanks for installing the Bottom of every post plugin by Corey Salzano. Contact me if you need custom WordPress plugins or website design.

Kernicterus: Epidemiological Strategies for Its Prevention through Systems-Based Approaches

Presented in part at the NICHD Conference, Research on Prevention of Bilirubin-Induced Brain Injury and Kernicterus-From Bench to Bedside, at Bethesda, Md, USA, June 2003.

Abstract

Kernicterus, thought to be due to severe hyperbilirubinemia, is an uncommon disorder with tragic consequences, especially when it affects healthy term and near-term infants. Early identification, prevention and treatment of severe hyperbilirubinemia should make kernicterus a preventable disease. However, national epidemiologic data are needed to monitor any preventive strategies. Recommendations are provided to obtain prospective data on the prevalence and incidence of severe hyperbilirubinemia and associate mortality and neurologic injury using standardized definitions, explore the clinical characteristics and root causes of kernicterus in children identified in the Kernicterus Pilot Registry, identify and test an indicator for population surveillance, validating systems-based approaches to the management of newborn jaundice, and explore the feasibility of using biologic or genetic markers to identify infants at risk for hyperbilirubinemia. Increased knowledge about the incidence and consequences of severe hyperbilirubinemia is essential to the planning, implementation and assessment of interventions to ensure that infants discharged as healthy from their birth hospitals have a safer transition to home, avoiding morbidity due to hyperbilirubinemia and other disorders.

At a recent NIHCD-sponsored conference, key questions were raised about kernicterus and the need for additional strategies for its prevention. These questions and an approach to their answers form the basis of this report.

A. IS KERNICTERUS A MATTER OF PUBLIC HEALTH CONCERN?

Available Evidence

Kernicterus has long been recognized as the pathologic sequela of severe hyperbilirubinemia. Although the condition is uncommon, the consequences are tragic, especially when it affects otherwise healthy term and near-term infants. Kernicterus has become uncommon because of effective screening for and prevention of Rh incompatibility, a historically important cause, and the accessibility of phototherapy to treat hyperbilirubinemia due to increased production and/or decreased elimination of bilirubin. Furthermore, adherence by clinicians to the guidelines from the American Academy of Pediatrics (AAP) concerning management of neonatal jaundice was expected to eliminate severe hyperbilirubinemia and prevent kernicterus.

Little contemporary information is available on the incidence or prevalence of kernicterus or its consequences. In the reports from the Pilot Kernicterus Registry and the Northern California Kaiser Permanente Medical Care Program (KPMCP) database, neonatal deaths due to kernicterus were ascertained from diagnostic codes on death certificates. Limitations of such observations include the retrospective design and possible under-reporting, delayed diagnosis, or errors in coding. For example, it is not feasible to estimate accurately a national incidence of kernicterus using the ICD-9 codes 773.4 and 747.7 for this diagnosis to query the HCUP database (Healthcare Cost and Utilization Project Agency for Healthcare Research and Quality, Rockville, MD; because the accuracy for annual reports is plusminus70 cases. That kernicterus occurs is evident from 125 cases of infants who had been discharged as healthy from their birthing hospitals that were voluntarily reported from 1992 to 2002 to the Pilot Kernicterus Registry. In contrast, no cases of kernicterus in infants with cerebral palsy were found in the retrospective database of KPMCP during a similar time period (1991 to 1998). In addition, among these 111,009 infants in the KPMCP database, 11 (0.01%) developed total serum bilirubin (TSB) levels greater than or equal to30 mg/dl, and none of them apparently developed kernicterus. However, it is unclear whether all cases were identified, since TSB was not routinely measured in all infants nor were these infants followed prospectively.

The actual incidences of kernicterus or severe hyperbilirubinemia are not available because neither is a reportable condition. The incidence of severe hyperbilirubinemia has been estimated  from a prospective study conducted in the 1960, a retrospective observational study of a population cared for in the 1990s, and additional prospective data from recent reports.  Rates of readmission after the birth hospitalization  range from 1.7 to 30.2 per 1000 live-births and represent a total of 42,470 readmissions for 1,532,924 live-births (27.7 per 1000) reported from 1988 to 1998.A disparity exists between term and near-term infants in the rates for readmission for jaundice. In a report of all California births from 1991 to 1999, C. Phibbs (personal communication) reported that near-term infants were consistently 6.4 to 6.6% of all well baby births (not admitted for neonatal intensive care), but their rate of readmission for treatment of jaundice was two- to three-fold higher than term infants

Figure 1.

Figure 1 - Unfortunately we are unable to provide accessible alternative text for this. If you require assistance to access this image, please contact help@nature.com or the authorRate of readmission for well babies for jaundice treatment in California (1991 to 1998) (California birth certificates were linked to the discharge abstracts for the birth hospitalization and readmission to identify the term and near-term well baby deliveries, and to separate readmissions for treatment of jaundice from those due to other causes.); data are presented for all well babies (filled diamond) and separated as term (filled circle) and near-term infants (filled triangle).

Research Recommendation

Obtain data on prevalence, incidence, and mortality of severe hyperbilirubinemia and associated neurologic injury, including kernicterus.

B. WHAT IS THE RELATIONSHIP BETWEEN SEVERE HYPERBILIRUBINEMIA AND KERNICTERUS?

Available Evidence

A spectrum of neuronal injury associated with hyperbilirubinemia is known as bilirubin-induced neurologic dysfunction (BIND). The spectrum ranges from subtle or suspicious extrapyramidal or other manifestations to acute encephalopathy and chronic posticteric sequelae, although some of the signs are controversial.

Acute brain injury induced by bilirubin is associated with one or more posticteric sequelae in survivors. These are: (1) a movement disorder consisting of athetosis, dystonia, choreoathetosis, but also including spasticity and hypotonia, (2) auditory dysfunction consisting of deafness or hearing loss and auditory neuropathy or dys-synchrony, (3) oculomotor impairments, especially of upward gaze, and (4) dental enamel hypoplasia of the deciduous teeth.

Even though TSB is an important risk factor, bilirubin-induced brain injury and kernicterus cannot be defined on the basis of TSB alone. Factors including the albumin binding of bilirubin, hemolysis, gestational age, and genetic vulnerability modify the risk of kernicterus in an individual infant. However, there is a paucity of studies that evaluate the impact of these risk factors on the incidence of BIND or the occurrence of subtle sequelae or transient neurologic abnormalities.

Contemporary prospective population-based studies that describe the natural history of hyperbilirubinemia are unavailable; data are limited to studies before the advent of phototherapy. In addition, no prospective studies relate the incidence of kernicterus associated with specific TSB values.Thus, characterizing the risk of brain injury at specific levels of TSB is problematic. Furthermore, the safe level of TSB, below which BIND does not occur in otherwise healthy jaundiced infants, is not known. A standard definition of kernicterus in term and near-term infants is needed for purposes of research. This could include a threshold value for TSB, for example, greater than or equal to20 mg/dl, plus abnormalities of muscle tone on neurological examination, auditory neurophysiological testing, and magnetic resonance imaging.

Research Recommendations

  1. Standardize definitions of severe hyperbilirubinemia, BIND, acute bilirubin encephalopathy, kernicterus. Uniform terminology is needed to compare databases and examine outcomes.
  2. Determine the prevalence and incidence of severe hyperbilirubinemia and kernicterus to estimate the risk of kernicterus at specific levels of TSB for term and near-term infants.
  3. Determine whether making a specific TSB level a reportable condition will accomplish this purpose.
  4. Develop a case–control study of adequate size to delineate the role of bilirubin and other factors in the development of kernicterus.
  5. Define population-based standards to help predict severe hyperbilirubinemia or, as important, the absence of risk based on predefined peak TSB levels.

C. WHAT ARE THE CHARACTERISTICS AND THE ROOT CAUSES OF RECENT CASES OF KERNICTERUS?

Preliminary Data

Preliminary data were presented on 125 of the 142 cases in the United States (including uniformed services) from the Pilot Kernicterus Registry (1992 to October 1, 2002). These infants were discharged as healthy and were included for analysis if they exhibited clinical signs of acute bilirubin encephalopathy and/or posticteric sequelae, regardless of TSB level and comorbidities. Most cases (about 50%) were voluntarily reported by parents or anonymously by physicians or nurses. One limitation of the registry is that these cases of kernicterus likely represent only a portion of affected children. Another limitation is that the population of newborns at risk because of severe hyperbilirubinemia is unknown, so that estimates of incidence and prevalence are unreliable. On the other hand, consistent observations from the registry provide the basis of recommendations for safe practices in order to prevent severe hyperbilirubinemia and kernicterus.

Characteristics of the population reported to the Pilot Kernicterus Registry (and individually listed in Appendix) included 84 male and 38 female cases, a racial distribution of White (58.4%), Black (26.4%), Hispanic (8.8%), Asian (6.4%) and the mean birth weight of 3281 g (range: 2015 to 4730). The mean gestational age was 38 weeks (range: 35 to 42.5). The etiology of hyperbilirubinemia in these infants, as evaluated upon readmission that was usually before 10 days of age, is listed in Table 3. All showed an excessive estimated rate of TSB rise (>0.20 mg/dl/hour) from birth to readmission. Analysis of these cases suggests the following root causes:(a) loss or lack of concern by clinicians regarding the neurotoxic potential of bilirubin, (b) limitations on visual recognition of jaundice as an index to initiate further evaluation or estimate severity, (c) failure to recognize the severity of hyperbilirubinemia at a specific age in hours; (d) failure to ensure appropriate follow-up 1 to 2 days after early discharge (24 to 72 hours of age); (e) delay in intensive or timely interventions before discharge or at readmission. More extensive analysis is needed of cases of kernicterus and predefined levels of severe hyperbilirubinemia (“close calls”) in order to better assess the performance of health-care providers and help address Institute of Medicine concerns, including patient (and family) centered care, quality of care, and patient safety.

Research Recommendations

  1. Conduct a comprehensive analysis of Registry cases to identify common characteristics, delineate the lapses in care that may have contributed to the occurrence of kernicterus, and determine the sentinel events that may have predicted the occurrence of kernicterus.
  2. Test the hypothesis that severe hyperbilirubinemia or kernicterus that affects babies discharged as healthy can be predicted before discharge.
  3. Assess the feasibility of a national reporting system and database for cases of pre-defined severe hyperbilirubinemia and kernicterus.
  4. Assess the feasibility of developing a systematic centralized review process, including root cause analysis, for prospective reported cases of severe hyperbilirubinemia that can be subsequently used to develop targeted education and systems improvements.
  5. Develop measurement tools to assess whether a centralized review process and interventions improve outcome.

D. WHAT SHOULD THE TARGET INDICATOR BE FOR PUBLIC HEALTH SURVEILLANCE OF KERNICTERUS AND/OR HYPERBILIRUBINEMIA?

At present, severe hyperbilirubinemia remains the most plausible surrogate indicator for kernicterus even though the risk of kernicterus at specific TSB ranges is estimated by clinical consensus rather than evidence-based criteria (Table 4). Surveillance for severe hyperbilirubinemia has distinct advantages. It describes an at-risk population, similar to identifying a population with hypertension regardless of its cause or its clinical outcome. TSB results are immediately available and objective, and can be reported rapidly. The inclusion of all cases, rather than just those with sequelae, would allow study of the risk of kernicterus in a population with hyperbilirubinemia, as well as study of the frequency and effects of any intervention. The TSB level at which cases might become reportable can be adjusted up or down based on risk and benefits. The immediacy and greater frequency of this outcome also make it potentially more useful for quality improvement efforts. Any initiative to begin surveillance for severe hyperbilirubinemia should be accompanied by efforts to improve standardization and minimize inter-laboratory variability.20

In general, there are at least four possible targets for public health surveillance related to kernicterus (Table 5). The first consideration is kernicterus itself. This disorder is the focus of current concern. However, the diagnosis may be delayed or under-reported. In addition, occurrences of kernicterus may be too infrequent (and too late) to provide feedback to health-care systems and providers that might reduce the risk of future cases. Surveillance for kernicterus would not capture other adverse effects of hyperbilirubinemia, including less typical sequelae and complications of exchange transfusion.

Like kernicterus, cerebral palsy is a highly relevant and clinically significant indicator. The diagnosis of cerebral palsy is already a matter of public health concern. Surveillance for cerebral palsy would allow studies of risk in children with different TSB levels, including those in whom TSB was never measured. However, the proportion of cerebral palsy due to kernicterus is not known, surveillance for cerebral palsy may be insensitive to changes in kernicterus incidence, and feedback to providers would be nonspecific and delayed.

Yet another surveillance strategy could be to monitor rates of readmission for treatment of hyperbilirubinemia or use of home phototherapy. Concomitant with incidence of severe hyperbilirubinemia, these offer useful indices of occurrence and outcome. On the other hand, interpretation is limited because intervention thresholds for severe hyperbilirubinemia have not been yet standardized.

Recommendations

  1. Identify an appropriate target indicator(s) for surveillance based upon advantages and disadvantages (Table 5).

E. HAVE SYSTEMS-BASED APPROACHES FOR THE MANAGEMENT OF NEWBORN JAUNDICE BEEN VALIDATED?

Available Evidence

Because of the concern for the reemergence of kernicterus,AAP and JCAHO recommend a universal systematic approach to the management of newborn jaundice, with the aim of reducing the incidence of severe hyperbilirubinemia and kernicterus. This involves using clinical risk factors analysis and/or measurement of predischarge TSB levels plotted an hour-specific nomogram to target appropriate follow-up and intervention. No prospective studies have compared or confirmed the effectiveness of such approaches. Whether a public health campaign to increase parental and provider awareness of jaundice and its potential consequences would reduce adverse outcomes is also unknown.

Research Recommendations

  1. Evaluate the recommendations for systems-based approaches for the prevention and management of severe hyperbilirubinemia. Approaches based on risk factors for severe hyperbilirubinemia or predischarge hour-specific TSB measurements should be prospectively validated for safety, costeffectiveness, and applicability to ethnically and racially diverse populations.
  2. Assess whether systematic prediction of severe neonatal hyperbilirubinemia prevents kernicterus in a cost-effective, practical and safe manner.
  3. Evaluate the epidemiologic impact of a public health campaign to reduce adverse outcomes of severe neonatal hyperbilirubinemia.

F. ARE THERE BIOLOGICAL OR GENETIC MARKERS THAT CAN BE USED TO BETTER DEFINE INFANTS AT RISK FOR SEVERE HYPERBILIRUBINEMIA?

Insufficient Evidence

The genetic contribution to neonatal hyperbilirubinemia due to disorders of hepatic bilirubin conjugation and to the pathogenesis of neuronal cell injury caused by hyperbilirubinemia needs further investigation.For example, early jaundice is greater in newborns homozygous for the polymorphism associated with Gilbert syndrome compared to those with the normal sequence or heterozygous for the mutation.The incidence of hyperbilirubinemia is also increased in infants who have the Gilbert polymorphism and glucose-6-phosphatase dehydrogenase (G6PD) deficiency. An investigation of microarray gene expression of hereditary disorders of unconjugated hyperbilirubinemia such as Gilbert, Arias, and Crigler-Najjar syndromes may elucidate possible coinheritance with G6PD deficiency, beta-thalassemia, and hereditary spherocytosis and identify infants at increased risk of severe hyperbilirubinemia. At this stage, it is too early to know whether genetic epidemiology of hyperbilirubinemia would contribute to the prevention of BIND.

Research Recommendation

Explore the feasibility of using diagnostic oligonucleotide microarrays for the known mutations of target genes to identify infants at increased risk of severe hyperbilirubinemia or those who have sustained kernicterus.

CONCLUSION

Infants discharged as healthy from their birth hospitals should have a safe transition to home, avoiding morbidity due to jaundice and other disorders. Prevention of readmission for severe hyperbilirubinemia in otherwise healthy infants, acute bilirubin encephalopathy, and chronic posticteric sequelae is a matter of public health and societal concern. Accurate data on the incidence of severe neonatal hyperbilirubinemia and associated adverse outcomes are fundamental to the planning, implementation, and assessment of interventions, including public policy and educational programs, to prevent adverse outcomes.

Thanks for installing the Bottom of every post plugin by Corey Salzano. Contact me if you need custom WordPress plugins or website design.

Fat lab lock-in: Can spicy pills help you lose weight?

What it’s like to run a gauntlet of metabolism tests to aid research into a spice-based pill designed to trick the body into burning off excess fat

See more in our gallery: “A human guinea pig in the brown fat lab

IT’S early evening, and I’m facing a dilemma of some delicacy – whether or not to break wind. Let me explain…

I’m poised to be voluntarily trapped in a room for the night as part of research to find new treatments for obesity at the Wellcome Trust Clinical Research Facility at Addenbrooke’s Hospital in Cambridge, UK. The aim of the experiment is to see if brown fat, a special type of fat tissue that turns energy obtained from food into heat, can be coaxed into burning more unwanted white fat than usual. They intend to do this using a simple food supplement – a daily capsule of spicy ingredients such as chilli pepper or cinnamon – aimed at mimicking the effects of being in the cold.

Recruited as a control, I’ve spent the afternoon undergoing a battery of tests to serve as reference data for how people in reasonably good health burn energy. Investigator Andy Whittle at the University of Cambridge explains that comparisons with this data will help establish whether people burn more energy than normal when kept in the cold (at 18 °C for 2 hours) or when given the spicy food capsules.

I will be confined to a special room for the night, which serves as a human-scale calorimeter. “We’ll treat you as if you’re a fire, measuring how much oxygen you take in and how much carbon dioxide you breathe out,” says Peter Murgatroyd, who designed the calorimeter. In other words, they will be capturing everything that goes in and out of my body.

Hence my dilemma. My fear is that by morning, thanks to forces beyond my control, the room will be embarrassingly uninhabitable. Being British, I’m too shy to ask about this but, eventually, I will inevitably yield to the growing pressure in my tummy and hope no one notices in the morning.

I have earned tonight’s sleep after this afternoon’s flurry of activity, which extracted every last ounce of information about how efficiently I expend energy. Near-naked inside an egg-shaped capsule called the Bodpod, I learned the relative amounts of fat and lean tissue in my body. A dual-energy X-ray absorptiometer informed me that I have 6 per cent less fat than normal for my age, with my bone density spot on. Then I was whisked off to a treadmill to see how efficiently I use oxygen while exercising.

Finally, the calorimeter beckons, where Whittle explains the rationale behind the research before my lock-in for the night. His aim is to subtly turn up the body’s central heating, taking lipid “fuel” from the bloodstream and from white fat cells that store it and send it for incineration in brown fat cells. Experiments in rodents have shown that the colder it is, the more energy they burn off in this way to produce heat. As babies, we also use this system to produce heat. But there is increasing evidence that many adults retain enough active brown fat, or adipose tissue, to do it too.

Whittle reckons this process is controlled by the brain, which orders the extra burning of fat in brown adipose tissue when it gets cold. Recent research has revealed that spicy food – such as cinnamon or capsaicin in chilli peppers – can activate nerve receptors in the skin, gut and mouth, triggering the same brain response as being cold does.

Whittle’s colleague Maarten Soeters cites findings from Japan published this year showing that men with active brown adipose tissue burn more energy than normal when given capsules of capsinoid compounds, similar to capsaicin (American Journal of Clinical Nutrition, DOI: 10.3945/ajcn.111.018606).

Now, Whittle is hoping to see if a mixture of ingredients like capsaicin can trick the brain into thinking it is cold, and coax brown adipose tissue into burning just a little more fat than normal, helping people to lose weight over years. He is keeping the exact ingredients secret for now.

“People get obese through a lifestyle that persists for years, yet we expect weight-loss treatments to work in months,” says Whittle. “The cause has been slow-drip, and your body doesn’t notice the rise in intake and a lack of exercise, so the trick to weight loss might be slow-drip in the other direction.”

I’m proud to have been able to help, but in the morning I can’t resist revisiting last night’s dilemma. Laura Watson, the physiologist who took my measurements, guffaws at my enquiry. “Don’t worry,” she says, “we’re used to it.”

Thanks for installing the Bottom of every post plugin by Corey Salzano. Contact me if you need custom WordPress plugins or website design.

A reproduction conundrum: For sperm, faster isn’t always better

0

When it comes to sperm meeting eggs in sexual reproduction, conventional wisdom holds that the fastest swimming sperm are most likely to succeed in their quest to fertilize eggs. That wisdom was turned upside down in a new study of sperm competition in fruit flies (Drosophila melanogaster), which found that slower and/or longer sperm outcompete their faster rivals.

The study, recently published online in Current Biologyand forthcoming in print on Sept. 25, was done by a team of scientists led by corresponding author Stefan Lüpold, a post-doctoral researcher in the Department of Biology in the College of Arts and Sciences. The team made the discovery using fruit flies that were genetically altered so that the heads of their sperm glow fluorescent green or red under the microscope. The fruit flies, developed by biology Professor John Belote, enable researchers to observe sperm in real time inside the female reproductive tract.

“Sperm competition is a fundamental biological process throughout the animal kingdom, yet we know very little about how ejaculate traits determine which males win contests,” says Lüpold, a Swiss National Science Foundation Fellow working in the laboratory of biology Professor Scott Pitnick. “This is the first study that actually measures sperm quality under competitive conditions inside the female, allowing us to distinguish the traits that are important in each of the reproductive phases.”

The research is also significant because the scientists studied naturally occurring variations in sperm traits, rather than manipulating the test populations for specific traits. After identifying and isolating groups of males with similar ejaculate traits that remained constant across multiple generations, the scientists mated single females with pairs of males from the different groups. “This approach allowed us to simultaneously investigate multiple ejaculate traits and also observe how sperm from one male change behavior depending upon that of rival sperm,” Lüpold says.

Female fruit flies mate about every three days. Sperm from each mating swim through the female bursa into a storage area until eggs are released. Eggs travel from the ovaries into the bursa to await the sperm. However, sperm battles actually take place within the storage area. After each mating, new sperm try to toss sperm from previous matings out of storage. The female then ejects the displaced sperm from the reproductive system, eliminating the ejected sperm from the mating game. The researchers observed that longer and slower-moving sperm were better at displacing their rivals and were also less likely to be ejected from storage than their more agile counterparts.

“The finding that longer sperm were more successful is consistent with earlier studies,” Lüpold says. “However, the finding that slower sperm also have an advantage is counterintuitive.”

Why slower sperm have an advantage is still open to speculation. “It could be that, when swimming back and forth in storage, slower sperm hit the exit less frequently and are therefore less likely to be pushed out,” Lüpold says. “Or, because sperm velocity is dependent on the density of sperm within the narrow storage area, it could be that velocity isn’t really the target of sexual selection in fruit flies, but is rather a consequence of the amount of sperm packed into the storage organ.”

###

Syracuse University: http://www.syr.edu

Thanks to Syracuse University for this article.

Thanks for installing the Bottom of every post plugin by Corey Salzano. Contact me if you need custom WordPress plugins or website design.