What happens in your brain when you have bipolar disorder

I love studies like this. They help substantiate that diagnoses such as bipolar disorder are not just "behavioral problems." They come with true biochemical imbalances, that sometimes even affect the tissue structure of the brain. Hopefully, the more studies like this are done, the less people with bipolar disorder will be looked down upon by society, and will be able to get the care they need that truly corrects these imbalances.

In this study, the fatty acid composition of the orbitofrontal cortex was studied in 10 patients with bipolar disorder. Compared to 19 cortices in individuals who did not have bipolar disorder. (This was performed in post-mortem, or after all the patients had died.)

Those individuals who had had bipolar disorder had higher concentrations of arachidonic acid and lower concentrations of docosahexaenoic acid (DHA) than those who had not. In both populations, there was also a trend toward higher arachidonic acid concentration and lower DHA concentration that was related to the degree of alcohol consumption.

A little visit over to Wikipedia gave me this information about the orbitofrontal cortex: Destruction...typically leads to a pattern of disinhibited behaviour. Examples include swearing excessively, hypersexuality, poor social interaction, compulsive gambling, excessive alcohol / smoking / drug use, and poor empathising ability. Disinhibited behaviour by patients with some forms of frontotemporal dementia is thought to be caused by degeneration of the OFC[8]. Patients with damage to the OFC tend to make rash decisions, and typically manage their finances poorly.

Sometimes it's easy to make judgments about a person's behavior and assume the person can just change them if they want to. It's reality that sometimes the problem is truly biological and that changing the nutritional status and/or the biochemistry of the brain is what is needed in order to help change behaviors.

McNamara RK, Jandacek R, Rider T, Tso P, Stanford KE, Hahn CG, Richtand NM. Deficits in docosahexaenoic acid and associated elevations in the metabolism of arachidonic acid and saturated fatty acids in the postmortem orbitofrontal cortex of patients with bipolar disorder. Psychiatry Res. 2008 Sep 30;160(3):285-99. Epub 2008 Aug 20.

Omega-3's for schizophrenia

DHA is commonly the omega-3 of the fish oils that gets the most attention for use in mental health conditions. However, EPA is gaining quite a reputation of its own. In this study, 24 patients presenting with their first episode of psychosis were treated with EPA for 12 weeks. Just before and at the end of this interval, brain scans were done to look for changes. Increases in glutathione and decreases in negative symptoms were observed as a result of EPA treatment.

Glutathione is a chemical that helps to prevent cell death, so its increase means EPA helps to preserve brain tissue. Because glutathione is not something that is easily administed via diet or supplementation, it's good to know there are other avenues for increasing its concentrations in populations at risk for greater rates of cell death, such as people with schizophrenia.

Berger GE, Wood SJ, Wellard RM, Proffitt TM, McConchie M, Amminger GP, Jackson GD, Velakoulis D, Pantelis C, McGorry PD. Ethyl-eicosapentaenoic acid in first-episode psychosis. A 1H-MRS study. Neuropsychopharmacology. 2008 Sep;33(10):2467-73. Epub 2008 Jan 16.

Why you can't just take a pill to feel better

Ohhh...I hate to say it, but we've become so lazy as a society. Evidence abounds that food, activity, stress management, and sleep choices can significantly affect overall health. But if given the option to try these or pay money for a pill or a medical procedure, the average American will tend to opt for the more passive option. Here's why those who make that choice may be selling themselves short.

Both omega-3 fatty acids and exercise have been found to improve brain function and keep brain tissue young.

A group of researchers is reporting that when the two are combined, compounds common in healthy, regenerating brain tissue (brain derived neurotrophic factor, or BDNF, for example) are higher than when only one of those options is applied. It seems as though the two play off of each other and each makes the other more effective.

Sorry, guys, there's no such thing as a way out of exercise and all the great things it does for you! :)

Wu A, Ying Z, Gomez-Pinilla F. Docosahexaenoic acid dietary supplementation enhances the effects of exercise on synaptic plasticity and cognition. Neuroscience. 2008 Aug 26;155(3):751-9.

A natural antipsychotic?

l-Stepholidine is a chemical derived from the Chinese herb Stephania. Since it had been found to have dopamine activity similar to that seen in atypical antipsychotics, it was tested and compared to the activity of haloperidol (Haldol) and clozapine (Clozaril). Scientists predicted its activity would more closely resemble clozapine. Indeed, when tested, it did mimic clozapine. The one downside researchers did report was that it was eliminated fairly rapidly from the body, which would make it challenging to use as a long-term therapeutic agent for treating schizophrenia.

What is stepholidine? It is a naturally occurring chemical, extracted from Stephania intermedia, a Chinese herb. I like to find pictures of herbs to share in this blog, but unfortunately, even Google can't pull anything up on this one.

I think this is exciting news, but being that this is very new information, I certainly am not recommending that anyone stop using a prescribed antipsychotic and head for Chinatown! I do promise, if anything new comes up, I'll be sure to share it in this blog along with references.

Natesan S, Reckless GE, Barlow KB, Odontiadis J, Nobrega JN, Baker GB, George SR, Mamo D, Kapur S. The antipsychotic potential of l-stepholidine--a naturally occurring dopamine receptor D1 agonist and D2 antagonist. Psychopharmacology (Berl). 2008 Aug;199(2):275-89.

When it takes more than a minute to describe how many medications you're taking...time to take a closer look.

Yesterday I was lunching with a dear friend, who mentioned that one of HIS friends has started to have problems with diabetes. I knew this friend also has Alzheimer's disease, so, knowing that many brain and nervous system-targeted medications can provoke insulin resistance and diabetes, I started asking questions about this person's medications.

We called the friend we were discussing for a complete list. Sure enough, in the battery of medications he had been prescribed...was valproic acid, or Depakote. Depakote is well documented to promote the development of metabolic syndrome--a cluster of problems including hypertension, insulin resistance, diabetes, and high cholesterol. Much of the research in this area has focused on women, because polycystic ovary syndrome, a feminine variant of metabolic syndrome, is also correlated with Depakote use. If you're looking for research on the effects of Depakote in men, it's there, it's just a little harder to find.

New research is suggesting that there is a link between diabetes and Alzheimer's disease. Some researchers even call it diabetes of the brain, and there is some evidence to suggest that diabetes medications such as metformin can help delay the progression of Alzheimer's syndrome.

So here we have a guy who has been prescribed a seizure medication, which has likely provoked his problems with diabetes, which is likely worsening his Alzheimer's disease...and what do you know? It seems as though now that he is on galantamine (Reminyl) for his Alzheimer's disease, he's started noticing tremors. I'd bet money on the possibility that the seizure meds are adjusted upward as a result.

So you can see where I'm going. Not only does this keep this poor guy's physicians busy, it pads the pockets of more than one pharmaceutical company, in progressively more expensive chunks.

My friend asked me what I would do? Well, I must qualify that I am not a prescribing medical doctor. I am a registered dietitian who studies the brain and nervous system. But this is where I'd go.

1. Based on the evidence that seizure disorders respond well to omega-3 fatty acids, I'd up those to a DHA equivalent of 1000 mg per day.
2. To help those omega-3's be most effective, I'd teach this person my "S" and "C" rule (avoid, as much as possible, all fats and oils beginning with the letters "S" and "C"...canola being the only exception). I know my friend and his friend eat out quite a bit and it likely is a significant source of these oils.
3. If you reduce the seizure and tremor activity, you reduce the need for seizure medication, and minimizing medications is always very important.
4. I would consider an alternative seizure medication with less potential for disrupting hormone balance. The one that I have seen repeatedly and successfully used in women to achieve this is lamotrigine (Lamictal). Of course, there may be a reason we do not know of that this would not be appropriate, but if this has not been considered it's certainly worth a try.
5. Less Depakote (or potentially no Depakote) potentially also means less insulin resistance, which provides the possibility that the Alzheimer's medication could be reduced. Again, less meds....fewer side effects.
6. Finally, acetyl l-carnitine has been shown to effectively reduce symptoms of diabetes as well as Alzheimer's disease. It also improves cholesterol profiles. And...it has repeatedly and specifically been found to effectively counter the negative side effects of Depakote. I have seen this cited so often recently I can't understand why it is not automatic for any physician prescribing Depakote to simultaneously recommend carnitine.

This trend, of treating one symptom, letting side effects develop, then treating them with other meds that create other side effects, which eventually build vicious cycles of ever-increasing doses of medications...in recent years...has spiraled out of control. The field of nutritional psychiatry is just out of the starting gate. But I'm hooked on its potential. Hopefully in this case, and for others who find this blog, we can help back our friends out of these pharmaceutical corners, save them some money, and improve their overall quality of life.



Luef G, Abraham I, Trinka E, Alge A, Windisch J, Daxenbichler G, Unterberger I, Seppi K, Lechleitner M, Kramer G, Bauer G. Hyperandrogenism, postprandial hyperinsulinism and the risk of PCOS in a cross sectional study of women with epilepsy treated with valproate. Epilepsy Res 2002 Jan;48(1-2):91-102.

Tan H, Orbak Z, Kantarci M, Kocak N, Karaca L. Valproate-induced insulin resistance in prepubertal girls with epilepsy. J Pediatr Endocrinol Metab 2005 Oct;18(10):985-9.

Aydin K, Serdaroglu A, Okuyaz C, Bideci A, Gucuyener K. Serum insulin, leptin, and neuropeptide y levels in epileptic children treated with valproate. J Child Neurol 2005 Oct;20(10):848-51.

Pylvanen V, Pakarinen A,Kniop M, Isojarvi J. Insulin-related metabolic changes during treatment with valproate in patients with epilepsy. Epilepsy Behav 2006 May;8(3):643-8.

Isojarvi JI, Laatikainen TJ, Pakarinen AJ, Juntunen KT, Myllyla VV. Polycystic ovaries and hyperandrogenism in women taking valproate for epilepsy. N Engl J Med 1993 Nov 4;329(19):1383-8.

Rasgon NL, Reynolds MF, Elman S, Saad M, Frye MA, Bauer M, Altshuler LL. Longitudinal evaluation of reproductive function in women treated for bipolar disorder. J Affect Disord 2005 Dec;89(1-3):217-25.

Roste LS, Tauboll E, Morkrid L, Bjornenak T, Saetre ER, Morland T, Gjerstad L. Antiepileptic drugs alter reproductive endocrine hormones in men with epilepsy.  Eur J Neurol. 2005 Feb;12(2):118-24.

Pylvanen V, Pakarinen A, Knip M, Isojarvi J. Characterization of insulin secretion in Valproate-treated patients with epilepsy. Epilepsia 2006 Sep;47(9):1460-4. Neurology. 2008 Sep 2;71(10):750-7.

Beeri MS, Schmeidler J, Silverman JM, Gandy S, Wysocki M, Hannigan CM, Purohit DP, Lesser G, Grossman HT, Haroutunian V. Insulin in combination with other diabetes medication is associated with less Alzheimer neuropathology. Prescrire Int. 2007 Oct;16(91):197-8.

McCain KR, Sawyer TS, Spiller HA. Evaluation of centrally acting cholinesterase inhibitor exposures in adults. Ann Pharmacother. 2007 Oct;41(10):1632-7.

López-Pousa S, Garre-Olmo J, Vilalta-Franch J. [Galanthamine versus donepezil in the treatment of Alzheimer's disease] Rev Neurol. 2007 Jun 1-15;44(11):677-84.

Schrauwen E, Ghaemi SN. Galantamine treatment of cognitive impairment in bipolar disorder: four cases. Bipolar Disord. 2006 Apr;8(2):196-9.

Aarsland D, Hutchinson M, Larsen JP. Cognitive, psychiatric and motor response to galantamine in Parkinson's disease with dementia. Int J Geriatr Psychiatry. 2003 Oct;18(10):937-41.

Isojarvie JI, Rattya J, Myllyla VV, Knip M, Ovine R, Pakarinen AJ, Tokay A, Tapaneinen JS. Valproate, lamotrigine, and insulin-mediated risks in women with epilepsy. Ann Neurol 1998 Apr;43(4):446-51.

Ribacoba-Montero R, Martinez-Faedo C, Diaz C, Salas Puig J. [Remission of polycystic ovary syndrome associated with valproic acid in an epileptic female]. Rev Neurol 2003 Apr 1-15;36(7):639-42.

Bruno G, Scaccianoce S, Bonamini M, Patacchioli FR, Cesarino F, Grassini P, Sorrentino E, Angelucci L, Lenzi GL. Acetyl-L-carnitine in Alzheimer disease: a short-term study on CSF neurotransmitters and neuropeptides. Alzheimer Dis Assoc Disord. 1995 Fall;9(3):128-31.

Thal LJ, Carta A, Clarke WR, Ferris SH, Friedland RP, Petersen RC, Pettegrew JW, Pfeiffer E, Raskind MA, Sano M, Tuszynski MH, Woolson RF. A 1-year multicenter placebo-controlled study of acetyl-L-carnitine in patients with Alzheimer's disease. Neurology. 1996 Sep;47(3):705-11.

Sano M, Bell K, Cote L, Dooneief G, Lawton A, Legler L, Marder K, Naini A, Stern Y, Mayeux R. Double-blind parallel design pilot study of acetyl levocarnitine in patients with Alzheimer's disease. FASEB J. 1992 Dec;6(15):3379-86.

Want to get someone's attention? Mess with their head

In all the years I've been doing this work, I've noticed people gradually tune out messages about fitness, weight management, and exercise...at least the ones with meaningful, important information. Except when it comes to their brains.

This past weekend, for example, I ran a demo booth at a local Whole Foods store for one of my company's sponsors, Organic Bistro. A gentleman and his son stopped by, and I offered them some samples of salmon cakes. The man pretty much went off on me.

"I'm vegan. I'm 51 years old. I'm a professional athlete. Just look at this body. Look at my legs. Do I look like I need your food? If I didn't know what I was doing would I be in this condition?"

I let him rant, and accommodated, interestingly, his wish that his son get a sample of the food that in his mind was not good enough for him.

After he finished, I said to him, "You clearly take very good care of yourself. I'm curious, though, because I'm a sports nutritionist and even athletes seem to not be getting some really important information about nutrition. Did you know that omega-3 fatty acids have been found to delay and possibly prevent the progression of Alzheimer's disease? And that it is possible but not easy to get those omega-3's in a completely vegan diet?"

The man's posture slumped, his voice got quiet, and he said, "My wife has permission, if I ever go there...to shoot me."

Since he'd dug a hole for himself and everyone in the frozen food aisle had been drawn into this interchange because of its decibel level, he couldn't really ask for more information.

So I pulled him aside and suggested that on his own, in the privacy of his own cable connection, that he Google "omega-3" and "Alzheimer's" and draw his own conclusions.

I'm not sure why it is that we're ok with a few extra pounds, we can justify eating that piece of cake even if we've been diagnosed with diabetes and there is a possibility that poor dietary choices might even lead to amputation...or eating those potato chips even though we want a baby and the evidence suggests that trans fats interfere with fertility...

...but you mention the brain and you've got a whole new, motivated audience.

My guess is, that by the time I'd broken down my demo this athlete had already been online learning about Alzheimer's. And hopefully, by now, has been back to Whole Foods for some of those really tasty wild salmon cakes.

Just one gram, that's all it takes!

A couple of years ago I prescribed fish oil to a client with depression. Her psychologist told her my recommendation was not proven in the research. These days, I'd be able to counter with a lot more hard data.

For example, in one study, 35 depressed adults (about half women, half men) were divided into 3 groups and given 3 different doses of DHA, one of the omega-3 fatty acids found in fish oil. 83% of the group with the lowest dose responded to the DHA with decreased symptoms of depression! Higher doses did not seem to be as effective.

My guess is, there may be a threshold over which adding more therapy into the system exceeds the body's ability to use it. So even with fish oil, more is not better may not be the appropriate approach.

However, I do like knowing that even a little bit of this very available, very inexpensive, nonpharmacological treatment can have profound effects on a common and debilitating issue. It's worth a try!

Mischoulon D, Best-Popescu C, Laposata M, Merens W, Murakami JL, Wu SL, Papakostas GI, Dording CM, Sonawalla SB, Nierenberg AA, Alpert JE, Fava M. A double-blind dose-finding pilot study of docosahexaenoic acid (DHA) for major depressive disorder. Eur Neuropsychopharmacol. 2008 Sep;18(9):639-45. Epub 2008 Jun 6.

Some great information on how to choose the right kind of fish

One of the most common arguments/questions I receive about fish is whether or not it is safe to eat because of the mercury content.

Rather than reinvent the wheel, I thought I'd share a blog sent to me by Jennifer Wilmes, MS, RD, another fish-friendly dietitian who is trying to get the right information out there.

Hope this frees up some choices for you!

http://www.babygooroo.com/index.php/2008/09/09/gone-fishin/

Can good science really be half full?

One reason I probably gravitated into science is that I am a very logical thinker. I enjoy following topics such as politics but I don't enjoy debating them because I'm usually thinking, "Why don't these people do outcome measurements with their legislation and report on that when they run for re-election?" Politics simply isn't an evidence-based discipline.

I admit, I can be overly-evidence-based, as evidenced by my prolific referencing in this blog. But that is what I am trained to do as a scientist--come to conclusions based on evidence.

So when a study like this one comes up, I just shake my head. At Cornell, I would have been handed back a paper like this with a big, fat, red "D" on the top. I would have been asked to rewrite my conclusions based on the evidence. These guys got published!

Based on the observation that mirtazapine (Remeron) helped to improve respiratory measurements in stroke patients, a group of scientists decided to try giving Remeron to ten patients, without depression, who had sleep apnea but refused to use a continuous positive airway pressure (CPAP) machine. Editorial note: Those contraptions SUCK...do you blame them?

Here is how they reported their results.

"After 51.9 +/- 8.4 days, the RDI was either reduced (51.9% in "responders" who were identified arbitrarily by a reduction in RDI >/= 25% at any time point of the investigation) or increased (154.4% in "non-responders"). Mirtazapine administration was stopped in the four patients with increased RDI. "

Translation: After an average of 52 days, patients either got better or worse. If you read the fine print where we said we only had 10 subjects in this study, almost half of them got worse.

Mirtazapine may be a probably effective treatment in stroke survivors with obstructive sleep apnea who refuse nasal CPAP treatment. As it may worsen central and mixed sleep apnea, patients who receive mirtazapine to alleviate sleep apnea or to control post-stroke depression with sleep disturbances should be monitored for changes in breathing parameters during sleep.

There is more waffling in that first sentence than I heard in the Democratic and Republican Convention broadcasts combined. Maybe a "probably effective" treatment? If you had cancer and you went in to your doctor and he suggested major surgery, would you be ok with him telling you that maybe this surgery was a "probably effective" strategy? If you were paying $20,000 for an in-vitro fertilization, would you fork that money over if all your doctor had to tell you was that maybe what you were paying him to do was "probably effective"

Translation: We really need to say something good about this medication so we can get published and keep our grant, but it looks like the only way we're going to be able to do that is fill this abstract with long sentences that go in circles and hope readers are in too much of a hurry to do the math.

I used to curse under my breath at those "D"'s my scientific writing professor used to scrawl across the top of my hard-labored assignments. Now I'm grateful he did. Not because it helps me to write this blog, but because when I need to ask for help for any of my own personal medical conditions, I can be much more assertive and judicious about negotiating the course (I'm talking safety as well as effectiveness)of my treatment.

Brunner H. Success and failure of mirtazapine as alternative treatment in elderly stroke patients with sleep apnea-a preliminary open trial. Sleep Breath. 2008 Aug;12(3):281-5. Epub 2008 Mar 28

Modulation of serotonin transporter function during fetal development causes dilated heart cardiomyopathy and lifelong behavioral abnormalities.

While I've drifted into the topic of antidepressants, I thought I'd share this piece on using them when pregnant. Two different antidepressants, fluoxetine (Prozac) and fluvoxamine (Luvox) were given to pregnant mice. Luvox reportedly did not as easily cross the placenta as Prozac. (This means that Luvox was not as available to the developing baby as Prozac was.)

Most of the rats' babies that were prenatally exposed to Prozac died after birth of a type heart failure known as dilated cardiomyopathy. This is a condition in which the heart becomes enlarged and too weak to pump enough blood to the rest of the body. These rats also showed alterations in serotonin receptor levels in the raphe nucleus, the part of the brain that is in charge of serotonin release. There was also an increased incidence of behaviors in these mice indicating anxiety and depression.

If you are female and you are choosing to treat your depression with an antidepressant, and you are at an age where you can conceive, you may wish to discuss this study with your prescribing caregiver. Your medication decisions are affecting two people, both deserving of consideration.

Noorlander CW, Ververs FF, Nikkels PG, van Echteld CJ, Visser GH, Smidt MP. Modulation of serotonin transporter function during fetal development causes dilated heart cardiomyopathy and lifelong behavioral abnormalities. PLoS ONE. 2008 Jul 23;3(7):e2782.

If you fix the real problem...you just might fix the problem

I just love the conclusions scientists come to when they're encouraged to promote the concept that for every problem...there's a medication.

Here we have a research group who took a group of rats and exposed them to chronic, unpredictable stress. The rats started developing neuron profiles consistent with cell death. So did the researchers recommend that in situations where it appears that chronic, unpredictable stress may be causing functional issues and medical risk, to implement support that reduces that stress? Of course not, silly reader, why would they do that? Support doesn't fund research or salaries. Drug companies do.

And that is why desipramine (Norpramin) was researched as the answer to this problematic observation. Never mind that this medication has been associated with increased insulin and prolactin levels in some people, a new use for this medication which increases the bottom line has been reported...let's give a big whoo hoo for stockholders!

Way back when I worked for someone else who had no boundaries when it came to employees' expectations, I was expected to bring my own laptop computer to work and use it most of my workday to enter data. After awhile, since laptops really aren't ergonomically superior, I developed carpal tunnel in both wrists. I had been pitching the pretty reasonable concept that since every other manager at my level in this company had both a desktop computer and an administrative assistant that I was not afforded, that I should have them too. So when I developed a medical issue that appeared to be directly related to my not being heard with regard to this issue, I viewed the doctor visit as an opportunity to finally get the note I needed mandating a repetetive motion activity restriction.

Unfortunately, the physician I visited was employed by the same man. And he decided what I really needed was a medication to dampen the pain. Isn't pain supposed to be telling you something? That you need to stop doing what's making you hurt?

Aren't dying neurons telling you something? That maybe something is killing them?

This mentality, that we can ignore the source of the problem and put a chemical bandaid on it so we don't have to change unhealthy situations, sure makes a lot of money for some people.

Did you ever consider that such money can only be made if you agree to hand it over? Medications can't hurt you if you decide not to take them. I am not advocating throwing all of your prescriptions away, at all. I'm just encouraging you to know exactly WHY you're being given a prescription and to consider proven non-pharmaceutical options whenever possible.

I ended up walking out on this company. From what I hear, it took several rounds of burning out successors for them to realize the problem was not the work ethic of the employee in the position. It was the expectations of the position created by the person who didn't understand the cost savings involved when you spend a little more on healthy work environments that help to retain hard working people. Me and my now-healthy wrists have never looked back.

Bachis A, Cruz MI, Nosheny RL, Mocchetti I. Chronic unpredictable stress promotes neuronal apoptosis in the cerebral cortex. Neurosci Lett. 2008 Sep 12;442(2):104-8.

McIntyre RS, Soczynska JK, Konarski JZ, Kennedy SH. The effect of antidepressants on glucose homeostasis and insulin sensitivity: synthesis and mechanisms. Expert Opin Drug Saf 2006 Jan;5(1)157-68.

Guzek JW, Olczak S, Lewandowska A. The hypothalamic and neurohypophyseal vasopressor and oxytocic content as influenced by alpha-adrenergic blockade in stressed rats. Acta Physiol Pol 1985 May-Jun;36(3):193-200.

Why are cats and bipolar disorder showing up in the same blog post?

I volunteer for two different animal rescue groups here in Phoenix. I like to say that when things get tough with humans, I de-stress with the animals. As my friends in these organizations have realized what I do for a living, I've been presented with some interesting opportunities to combine both interests. You may have seen the post about Norm, the abandoned cat who we eventually lost due to consequences of prolonged and severe malnutrition. Thanks to my nutrition colleagues, I was steered toward a refeeding protocol developed by the World Health Organization used with children in third world countries. It's had limited and successful use in animals. I have submitted it to our vet staff for review, with the hopes that the next time an animal in need comes our way, we won't have to go through the emotional stress of losing it.

Last week, my friend Gerda paid me to consult with her about her cat Yani. I know Yani from the Arizona Animal Welfare League, and Gerda is a PhD candidate at Arizona State University. She is so diligent, she has plotted Yani's weight on a white board and kept his intake records over several months so we can problem solve. (Being the animal lover that she is, she put "anonymous" rather than "Yani" next to his assigned color so he wouldn't develop body image issues over being identified as obese!) So all of the medical and nutritional history I have for him makes this like a dream project in a fancy nutritional lab.

Despite Gerda's best efforts and documentation that Yani's food intake is limited, he continues to gain weight. He is, in turn, exhibiting signs and symptoms of depression. No interest in exercise. Extreme interest in food. Interest in food with any kind of environmental stimulation. I find this fascinating, because I used to work in eating disorders. Humans with eating disorders tend to connect all of their eating issues to some kind of psychological issue--an abuse, a trauma, an emotional issue. But here we have a cat, exhibiting the same behaviors and as far as we know he's not been verbally belittled, he's not had his body image assaulted by reading a few too many issues of Elle or Vogue, and he's certainly not being coerced by food ads on television. (Fortunately for Yani, and my Ivy League-ingrained insistence on maintaining proper scientific method, Gerda is more of a PBS than a Desperate Housewives person.)

So we've started a Facebook group and we're trying to figure out why Yani is getting fat when, thanks to a conscientious kitty mom and dad, he is following all the rules.

It seems, we've learned, that cats don't do well with carbohydrates. Many cat foods have carbohydrate fillers. And in reading cat food labels, I've seen supposedly high-protein foods that are high protein because they contain fillers such as corn gluten and soy protein that any self-respecting cat would never choose on his own. Cats are meat eaters. We've switched Yani primarily to meat, tossed the fillers, and we're experimenting with carnitine, a supplement that has been found to help metabolize fat and has actually been studied in cats.

I am particularly interested in what happens with Yani, because it's been my experience that people with mood disorders also seem to have problems with their weight. Some of it is binge eating, I know, but there just seems to be something metabolic that goes with a mood disorder that causes a proneness to gaining weight. It can even often be seen in the body type--solid center of gravity, proneness to gaining weight around the abdomen, skinny legs, in women, a tendency toward bustiness--it's the most common body type I treat in working with mental illness. I just described the apple shaped body type that is defined as a risk factor for metabolic syndrome, if you're not familiar with it. More and more, my observation is being supported in the literature, that people who have metabolic syndrome tend to have this body type...and to be more prone to mood disorders. This long drawn out dissertation is my attempt to be politically correct at saying that sometimes there is a genetic tendency toward a mood disorder, and that can be strongly linked with problems with weight.

When you see the issue manifest in a cat, who isn't subject to the same kind of emotional conditioning as a human, it really points to the fact that some people are, weight and calorie wise, completely different from others.

Researchers recently looked at the medical records of 161 individuals with bipolar disorder. Over three fourths of them were were overweight, and almost half were obese. High triglycerides, high blood pressure, and diabetes were noted at a rate greater than is observed in the general population. Over half met the criteria for metabolic syndrome.

There was a trend toward even greater incidence among individuals whose bipolar disorder was being managed with second generation antipsychotics (for example, Zyprexa). However, the trend existed whether or not those medications were part of the scenario.

My point? There are many psych meds that get blamed for weight gain. The reality is that they may exacerbate a pre-existing tendency toward weight gain, but they do not cause it. That genetic profile may benefit from a certain kind of diet. Just as Yani cannot blame his weight gain on poor social conditioning and must be encouraged to follow a lifestyle that minimizes his identified genetically-based medical risks, so must people with bipolar and other mood disorders. Weight gain is not necessarily an excuse to not take medications. A well-planned diet may help to minimize weight gain, and that is why it can be helpful to work with a nutritionist specializing in mental health, in conjunction with a psychiatrist who understands the complex interactions of mood, weight, and hormone function.

Fiedorowicz JG, Palagummi NM, Forman-Hoffman VL, Miller del D, Haynes WG. Elevated prevalence of obesity, metabolic syndrome, and cardiovascular risk factors in bipolar disorder. Ann Clin Psychiatry. 2008 Jul-Sep;20(3):131-7.

Special note: In order to continue to protect Yani's identity and self-image, the photo above is merely a stock photo of a random cat. The photo is included solely for illustrative purposes and is not intended to belittle or poke fun at any animal whose weight exceeds kitty culturally-accepted norms.

Hyperglycemia-induced membrane lipid peroxidation and elevated homocysteine levels are poorly attenuated by exogenous folate in embryonic chick brains

Today I wanted to share some recent findings about the effects of elevated glucose on a developing baby's nervous system. I often think we start too late when looking for origins of many medical issues. I've learned to start way back in utero when evaluating a situation and trying to sort through what's going on. Here's an example of why that can be important.

A group of chick eggs were injected with glucose. Significant changes were found in the babies that developed from those eggs, including:
--their own hyperglycemia
--elevated oxidative (degenerative) activity in body and brain tissue
--lower body weight
--lower brain weight
There also seems to be lower levels of DHA in babies exposed to hyperglycemia. This may be due to the elevated oxidative activity destroying any DHA that might be there.

You're likely aware that taking folate is pretty much an across the board recommendation to pregnant women. In this study, hyperglycemia seemed to induce a level of oxidation/inflammation that was not significantly helped with a folate supplement.

Bottom line, it's important to eat well not just to avoid weight gain or to keep your blood sugar low to keep your doctor and dietitian happy, but because your baby's brain and body depend on you to do so.

Most of my clients express surprise that healthy eating includes as many tasty foods as it does. So before you write off a visit to the dietitian because you're afraid of what you WON'T be able to eat, consider that it may be your ticket to freedom and guilt relief to work with someone who can introduce you to the many foods that will BENEFIT you and baby!

Cole NW, Weaver KR, Walcher BN, Adams ZF, Miller RR Jr. Hyperglycemia-induced membrane lipid peroxidation and elevated homocysteine levels are poorly attenuated by exogenous folate in embryonic chick brains. Comp Biochem Physiol B Biochem Mol Biol. 2008 Jul;150(3):338-43.