Monday, June 16, 2008

Momma was right--fish is brain food


Just a simple straightforward study that validates every mother in history who got out the cod liver oil and told her kids it was good for the brain. Eighty-five fourth graders receiving 400 mg per day of docosahexaenoic acid (DHA) were compared to 90 fourth graders who didn't, with regard to a battery of cognitive tests. There was a positive relationship between blood DHA levels and scores on the Peabody Picture Vocabulary Test, a test of listening comprehension and vocabulary acquisition.

Can't stand the thought of getting fish oil into your kids? Here are some nice options.

1. Coromega makes a pudding-type emulsion that tastes just like a Creamsicle. www.coromega.com.

2. Saturday I tasted tested a new product at a local health food store clearly made with kids in mind--Barlean's Omega Swirl lemon zest flavored fish oil emulsion. You'd never know it was fish, and 2 teaspoons contains 365 mg EACH of DHA and EPA. http://www.barleans.com/omega_swirl.asp

3. For kids who are way too assertive to trust anything that remotely resembles a supplement or a fish...Omega 3 Brain Booster Powder is a tasteless, odorless, water-soluble, heat stable, gluten-free fish oil powder blended into a rice protein base. You can bake with it, cook with it, stir it into your favorite juice. I've done some work for this company and we've tested it on boatloads of kids. They'll take it in anything...the caveat being you don't prompt them to decide they don't like what you're serving by telling them it has fish oil in it. Healthy spaghetti sauce...here we come! You can get 10% off your first online purchase of this particular product by going to www.omega3powder.com. A little note: The owner of the company recently chose to take a major hit on his revenues in order to maintain integrity and customer safety. The rice shortage had reduced his sourcing options for rice protein to imports from China and Denmark. Even though the Chinese option would have allowed him to continue production without disruption, he opted to let his supply run out and run into back order status, and wait for the Danish rice protein. That's one reason why I love working for this man, he'll never make money in a way that compromises the safety of anyone he truly wants to help with his work.

Ryan AS, Nelson EB. Assessing the effect of docosahexaenoic acid on cognitive functions in healthy, preschool children: a randomized, placebo-controlled, double-blind study. Clin Pediatr (Phila). 2008 May;47(4):355-62.

Saturday, June 14, 2008

Keeping your brains right where they belong

A few years ago I was working with a client with polycystic ovary syndrome. In the course of giving her medical history, she'd also disclosed that she had hyperprolactinemia, a condition in which milk production and let down occurs, even in men, and even in women who are not nursing, if their blood levels of prolactin are too high. She told me that she continued to produce and release milk for four years after delivering her last child, and not a single physician she'd asked about it here in Arizona or over in California seemed to think it was a situation worthy of medical intervention. So she lived with it, until it eventually went away.

As we progressed through our consultation, I explained to her why omega-3 fatty acids are so important--as they are an integral part of the brain's structure and functioning. I then explained to her that breast milk is high in omega-3 fatty acids, and that babies who are nursed are more likely to get these crucial fatty acids than babies on formula.

I looked up from my notepad to see my client red-faced. If steam could have come out of her ears, it would have.



Thinking I'd said something hurtful or offensive, I asked her if something was wrong.

She looked at me and asked, "So you mean to tell me...for four whole years...my brains were leaking out of my boobs and no one seemed to think that was a problem?"

I was the professional in that situation and so it fell on me to keep a completely straight face and answer a serious "yes, yes that's true."

Hyperprolactinemia really is a condition that needs to be taken seriously. As my client correctly deduced, it can drain the body of some of its most essential compounds, which can promote inflammation and potentially disrupt healthy brain function. Some psychiatric medications can increase the risk of hyperprolactinemia. One that has this reputation is risperidone (Risperdal).

A group of Chinese researchers recently tested an herbal remedy for hyperprolactinemia, peony-glycyrrhiza decoction, against a more traditional treatment, a medication called bromocryptine. Their subjects were women whose hyperprolactinemia was a direct result of risperidone use. For the purposes of this study, the women were also experiencing irregular periods (oligomenorrhea) or absence of periods (amenorrhea). Each group was exposed to both the herbal and the pharmaceutical treatment, with one group starting on herbs and switching to medication. The second group received the treatments in the reverse order. Psychotic symptoms, negative side effects, and levels of the hormones prolactin, estradiol, testosterone, and progesterone were all measured at the beginning and end of the study.

Not only did the herbal preparation produce a decrease in prolactin similar to the medication, other hormones were not affected, and psychosis was not worsened. And, more often in the herbal than the pharmaceutical remedy, there were improvements in negative side effects of hyperprolactinemia.

Whether or not you are on a medication, if you're producing breast milk and you are not nursing a baby, it is a medical problem and it does need to be addressed.

And now that you've read this post, you won't need to wait four years until a nutritionist mentions in passing that you should insist that your problem be taken seriously.

Yuan HN, Wang CY, Sze CW, Tong Y, Tan QR, Feng XJ, Liu RM, Zhang JZ, Zhang YB, Zhang ZJ. A randomized, crossover comparison of herbal medicine and bromocriptine against risperidone-induced hyperprolactinemia in patients with schizophrenia. J Clin Psychopharmacol. 2008 Jun;28(3):264-370.

Bowden CR, Voina SJ, Woestenborghs R, Do costerR, Heykants J. Stimulation by risperidone of rat prolactin secretion in vivo and in cultured pituitary cells in vitro. J Pharmacol Exp Ther 1992 Aug;262(2): 699-706.

Kinon BJ, Stauffer VL, McGuire HC, Kaiser CJ, Dickson RA, Kennedy JS. The effects of antipsychotic drug treatment on prolactin concentrations in elderly patients. J Am Med Dir Assoc 2003 Jul-Aug; 4(4): 189-94.

Lee BH, Kim YK. The relationship between prolactin response and clinical efficacy of risperidone in acute psychotic inpatients. Prog Neuropsychopharmacol Biol Psychiatry 2006 Jun;30(4):658-62.

Holzer L, Eap CB. Risperidone-induced symptomatic hyperprolactinaemia in adolescents. J Clin Psychopharmacol 2006 Apr;26(2):167-71.

Foley KF, Kast RE. Review of evidence that posttransplantation psychiatric treatment commonly affects prolactin levels and thereby influences graft fate. Gen Hosp Psychiatry 2006 May-Jun;28(3):230-3.

Anderson GM, Scahill L, McCracken JT, McDougle CJ, Aman MG, Tierney E, Arnold LE, Martin A, Katsovich L, Posey DJ, Shah B, Vitiello B. Effects of short- and long-term risperidone treatment on prolactin levels in children with autism. Biol Psychiatry 2007 Feb 15;61(4):545-50.

Staller J. The effect of long-term antipsychotic treatment on prolactin. J Child Adolesc Psychopharmacol 2006 Jun;16(3):317-26.

Madhusoodanan S, Moise D. Risperidone-induced hyperprolactinemia in adolescents: A case series. J Clin Psychiatry 2006 Jul;67(7):1110-3.

Meldersson KI. Prolactin elevation of the antipsychotic risperidone is predominantly related to its 9-hydroxy metabolite. Hum Psychopharmacol 2006 Dec;21(8):529-32.

Kopecek M, Bares M, Horacik J, Mohr P. Low-dose risperidone augmentation of antidepressants or anxiolytics is associated with hyperprolactinemia. Neuro Endocrinol Lett 2006 Dec;27(6):803-6.

Troost PW, Althaus M, Lahuis BE, Buitelaar JK, Minderaa RB, Hoekstra PJ. Neuropsychological effects of risperidone in children with pervasive developmental disorders: a blinded discontinuation study. J Child Adolesc Psychopharmacol 2006 Oct;16(5):561-73.

Eberhard J, Lindstrom E, Holstad M, Levander S. Prolactin level during 5 years of risperidone treatment in patients with psychotic disorders. Acta Psychiatry Scand 2007 Apr;115(4):268-76.

Bushe C, Shaw M. Prevalence of hyperprolactinaemia in a naturalistic cohort of schizophrenia and bipolar outpatients during treatment with typical and atypical antipsychotics. J Psychopharmacol 2007 Sep;21(7):768-73.

Duval F. Guillon MS, Mokrani MC, Crocq MA, Garcia Duarte F. Relationship between prolactin secretion, and plasma risperidone and 9-hydroxyrisperidone concentrations in adolescents with schizophreniform disorder. Psychoneuroendocrinology 2007 Nov 27.

Synek O, Svestka J, Tomanova J, Rodakova I, Cejpkova A. Differences in the effect of second-generation antipsychotics on prolactinaemia: Six weeks open-label trial in female in-patients. Neuro Endocrinol Lett 2007 Dec 6;28(6).

Togo T, Iseki E, Shoji M, Oyama I, Kase A, Uchikado H, Katsuse O, Kosaka K. Prolactin levels in schizophrenic patients receiving perospirone in comparison to risperidone. Neurology 2003 Apr 8;60(7): 1130-5.

Brunelleschi S, Zeppegno P, Risso F, Cattaneo CI, Torre E. Risperidone-associated hyperprolactinemia: evaluation in twenty psychiatry outpatients. Pharmacol Res 2003 Oct;48(4): 405-9.

Volavka J, Czobor P, Cooper TB, Sheitman B, Lindenmayer JP, Citrome L, McEvoy JP, Lieberman JA. Prolactin levels in schizophrenia and schizoaffective disorder patients treated with clozapine, olanzapine, risperidone, or haloperidol. J Clin Psychiatry. 2004 Jan;65(1):57-61.

Blogroll

OK, OK, I succumbed to the blogroll. I wasn't going to contribute to anyone's blog addiction and sore neck and shoulders, but some of my friends and supporters are writing great stuff I don't want you to miss if it should help you! So I've got a few options to get you started.

Only when it's 3 am and you're still sitting in front of your computer, it's your own lack of impulse control and not my reckless lack of editing discretion that your boss needs to hear about when you're caught napping at your desk the next day. :)

Between traveling/speaking 3 times in two cities in 5 days and reviewing the last month's worth of research abstracts, time for writing has been short. I should be back to getting you all some good abstracts starting Monday.

Happy Father's Day everyone!

Tuesday, June 10, 2008

I'll take a smoothie and a siesta over Ambien anytime

If you've ever dieted, and you have trouble sleeping...there may be a reason. Keep in mind, this study was done on rainbow trout, but there is still a message in it for humans. Three groups of trout were studied with regard to their melatonin (sleep hormone/antioxidant) levels and cortisol (stress hormone) levels. The three groups were defined as fed fish, fish that were fasted for 7 days, and fish that were fasted for 7 days then refed for 5 days.

Melatonin levels were disrupted in fasted fish. If you were human, this would likely mean if you were on a strict fasting/dieting protocol, you were probably having trouble sleeping as well.

Interestingly, nighttime serotonin levels were higher in these fasted fish. Melatonin is made from serotonin, so I would presume that what the body tries to do when you're not eating well is to keep you alert and thinking about getting some food. It does that by hanging on to serotonin and preventing its conversion into melatonin. That's a survival mechanism.

So if you're dieting and you're awake at night with cravings? That's a normal response. Don't obsess about what's wrong with you, don't surf the Internet looking for what to do about your cravings. In this kind of situation, you're thinking about food because you need it. Get some.

As far as cortisol, dieting reduced levels and they stayed low after refeeding. You could argue that this is a benefit of dieting...except for the fact that if you're cutting yourself short on melatonin, you're aging yourself more quickly than you should. There are plenyy of ways to reduce melatonin levels without dieting that don't cut your life short on the back end.

By the way, since I write so much about sleep I thought I should mention...I love naps. The long afternoon kind where my cats curl up with me, and I wake up with a little bit of drool on my pillow. I don't feel guilty at all. I completely buy into the idea of "beauty sleep"--sooooo much cheaper than all those anti-aging potions on the infomercials!

Ceinos RM, Polakof S, Illamola AR, Soengas JL, Míguez JM. Food deprivation and refeeding effects on pineal indoles metabolism and melatonin synthesis in the rainbow trout Oncorhynchus mykiss. Gen Comp Endocrinol. 2008 Apr;156(2):410-7. Epub 2008 Jan 8.

Friday, June 6, 2008

Survey says...

I'm six months into writing this blog, and I took some time to look at the statistics this morning. I am interested to know what interests all of you readers so that I can provide more of that. It was a bit of a shot in the dark at first, guessing what would bring you in to read my thoughts, but I do have a bit more of an idea as time goes on.

The ten most read pages were about: aspartame, topamax and off-label uses, fish oil/anxiety/anger, fibromyalgia, melatonin and REM sleep behavior disorder, topamax and kidney problems, rozerem and sleep apnea, vinpocetine, wheatgrass, olanzapine/stuttering.

The top ten search terms were: fish oil/anxiety, cellular effects of aspartame, acth/paxil, aspartame/depression, rozerem, rozerem/sleep apnea, epa/anxiety, topamax/binge eating, caffeine/antidepressants, olanzapine/stuttering.

So now I know what people found when they looked for it. What I don't know is...what were you looking for that you didn't find? That is something my statistics won't tell me. But if I know what you all wish to see, I can keep that in mind when I get my monthly pile of research from the Nat'l Library of Medicine.

I'm surprised at how many people not only found this blog, but return for more, and I'm delighted at how interactive it's become. I hope to bring more information to you all, and to be challenged to present science in a fun and meaningful way. Your responses and suggestions will definitely guide me toward making this the best possible resource on the 'net when it comes to psych meds.

Have a great summer weekend everyone!

Wednesday, June 4, 2008

Your blood pressure will rise over this one

I don't have to tell you that it's important to keep your blood pressure under control. And if you're intelligent enough to have interest in reading this blog, then you also know that if you're overweight, and your blood pressure is high, it is likely to drop if you take the steps to lose the weight.

Well, some scientists got a little muddled about why it's important to lose weight in the first place. And they developed this medication, sibutramine (Meridia), that is supposed to be a weight loss aid.

The only problem is, sibutramine doesn't help reduce blood pressure. In fact, in enough people so that it routinely shows up in the research literature, sibutramine has been observed to raise blood pressure. I've got twelve references about this in my drug book (listed below for your reference). In addition to raising blood pressure, elevated heart rate, insomnia, and agitation were also reported side effects.

MY blood pressure started to rise as I reviewed these references. Because I couldn't help but wonder if sibutramine would even be allowed on the market if it were a drug for cancer, or ulcers, or arthritis, and it caused hypertension, arrhythmia, and/or agitation? You can bet not.

But there is such a race to see who can create the magic weight loss pill that scientists seem to have forgotten why we even want people to lose weight. I can just see these Dr./patient interactions behind closed doors everywhere..."Well, Mr. Smith, the bad news is you can't sleep, your heart's racing, you're on the verge of a stroke, and you've annoyed the hell out of your family, friends, and coworkers with your new Type A personality. But hey, guess what? (Drum roll..........) You're THIN!!!"










HUH?!?!?

Your blood pressure isn't high because you have a Meridia deficiency. It's high because you have an activity and good food deficiency.

Is it just me, or is this a little bit like a scientific "Who's On First?"

Lechin F, van der Dijs B, Hernandez G, Orozco B, Rodriguez S, Baez S. Neurochemical, neuroautonomic and neuropharmacological acute effects of sibutramine in healthy subjects. Neurotoxicology 2006 Mar;27(2):184-91.

Avenell A, Brown TJ, McGee MA, Campbell MK, Grant AM, Broom J, Jung RT, Smith WC. What interventions should we add to weight reducing diets in adults with obesity? A systematic review of randomized controlled trials of adding drug therapy, exercise, behaviour therapy or combinations of these interventions. J Hum Nutr Diet. 2004 Aug;17(4):293-316.

Rucker D, Padwal R, Li SK, Curioni C, Lau DC. Long term pharmacotherapy for obesity and overweight: updated meta-analysis. BMJ 2007 Dec 8;335(7631):1194-9.

Di Francesco V, Sacco T, Zamboni M, Bissoli L, Zoico E, Mazzali G, Minniti A, Salanitri T, Cancelli F, Bosello O. Weight loss and quality of life improvement in obese subjects treated with sibutramine: a double-blind randomized multicenter study. Ann Nutr Metab 2007;51(1):75-81.

Hanotin C, Thomas F, Jones SP, Leutenegger E, Drouin P. Efficacy and tolerability of sibutramine in obese patients: a dose-ranging study. Int J Obes Relat Metab Disord 1998 Jan;22(1): 32-8.

Dunican KC, Desilets AR, Montalbano JK. Pharmacotherapeutic options for overweight adolescents. Ann Pharmacother 2007 Sep;41(9):1445-55.

Elliott WJ. Drug interactions and drugs that affect blood pressure. J Clin Hypertens (Greenwich). 2006 Oct;8(10):731-7.

Porter JA, Raebel MA, Conner DA, Lanty FA, Vogel EA, Gay EC, Merenich JA. The Long-term Outcomes of Sibutramine Effectiveness on Weight (LOSE Weight) study: evaluating the role of drug therapy within a weight management program in a group-model health maintenance organization. Am J Manag Care. 2004 Jun;10(6):369-76.

Faria AN, Ribeiro Filho FF, Kohlmann NE, Gouvea Ferreira SR, Zanella MT. Effects of sibutramine on abdominal fat mass, insulin resistance and blood pressure in obese hypertensive patients. Diabetes Obes Metab. 2005 May;7(3):246-53.

Perrio MJ, Wilton LC, Shakir SA. The safety profiles of orlistat and sibutramine: results of prescription-event monitoring studies in England. Obesity (Silver Spring). 2007 Nov;15(11):2712-22.

Berube Parent S, Prud’homme D, St. Pierre S, Doucet E, Tremblay A. Obesity treatment with a progressive clinical tri-therapy combining sibutramine and a supervised diet-exercise intervention. Int J Obes Relat Metab Disord 2001 Aug;25(8): 1144-53.

McMahon FG, Fujioka K, Singh BN, Mendel CM, Rowe E, Rolston K, Johnson F, Mooradian AD. Efficacy and safety of sibutramine in obese white and African American patients with hypertension: a 1-year double-blind, placebo-controlled, multicenter trial. Arch Intern Med 2000 Jul 24;160(14): 2185-91.

Weintraub M, Rubio A, Golik A, Byrne L, Scheinbaum ML. Sibutramine in weight control: a dose-ranging, efficacy study. Clin Pharmacol Ther 1991 Sep;50(3): 330-7.

Van Gaal LF, Wauters MA, Peiffer FW, De Leeuw IH. Sibutramine and fat distribution: is there a role for pharmacotherapy in abdominal/visceral fat reduction? Int J Obes Relat Metab Disord 1998 Aug; 22 Suppl 1:S38-40; discussion S41-2.

Hanotin C, Thomas F, Jones SP, Leutenegger E, Drouin P. A comparison of sibutramine and dexfenfluramine in the treatment of obesity. Obes Res 1998 Jul;6(4): 285-91.

Fanghanel G, Cortinas L, Sanchez-Reyes L, Berber A. A clinical trial of the use of sibutramine for the treatment of patients suffering essential obesity. Int J Obes Relat Metab Disord 2000 Feb; 24(2): 144-50.

Bailey DG, Dresser GK. Interactions between grapefruit juice and cardiovascular drugs. Am J Cardiovasc Drugs. 2004;4(5):281-97

Xu J, Chen JD. Peripheral mechanisms of sibutramine involving proximal gastric motility in dogs. Obesity (Silver Spring). 2006 Aug;14(8):1363-70.

Connoley IP, Liu YL, Frost I, Reckless IP, Heal DJ, Stock MJ. Thermogenic effects of sibutramine and its metabolites. Br J Pharmacol 1999 Mar,126(6): 1487-95.

Derosa G, Cicero AF, Murdolo G, Ciccarelli L, Fogari R. Comparison of metabolic effects of orlistat and sibutramine treatment in Type 2 diabetic obese patients. Diabetes Nutr Metab. 2004 Aug;17(4):222-9.

Gokcel A, Karakose H, Ertorer EM, Tanaci N, Tutuncu NB, Guvener N. Effects of sibutramine in obese female subjects with type 2 diabetes and poor blood glucose control. Diabetes Care 2001 Nov; 24(11): 1957-60.

Hauner H, Meier M, Wendland G, Kurscheid T, Lauterbach K, Study Group SA; SAT Study. Weight reduction by sibutramine in obese subjects in primary care medicine: the SAT Study. Exp Clin Endocrinol Diabetes. 2004 Apr;112(4):201-7.

McNeely W, Goa KL. Sibutramine. A review of its contribution to the management of obesity. Drugs 1998 Dec;56(6): 1093-24.

Fanghanel G, Cortinas L, Sanchez Reyes L, Berber A. Second phase of a double blind study clinical trial on sibutramine for the treatment of patients suffering essential obesity: 6 months after treatment cross-over. Int J Obes Relat Metab Disord 2001 May;25(5): 741-7.

Norris SL, Zhang X, Avenell A, Gregg E, Schmid CH, Lau J. Pharmacotherapy for weight loss in adults with type 2 diabetes mellitus. Cochrane Database Syst Rev. 2005 Jan 25;(1):CD004096.

Padwal R, Li SK, Lau DC. Long-term pharmacotherapy for obesity and overweight. Cochrane Database Syst Rev. 2004;(3):CD004094.

Fanghanel G, Cortinas L, Sanchez Reyes L, Berber A. Second phase of a double blind study clinical trial on sibutramine for the treatment of patients suffering essential obesity: 6 months after treatment cross-over. Int J Obes Relat Metab Disord 2001 May;25(5): 741-7.

Stimac D, Ruzic A, Majanovic SK. Croatian experience with sibutramine in the treatment of obesity--multicenter prospective study. Coll Antropol. 2004 Jun;28(1):215-21.

Appolinario JC, Godoy Matos A, Fontenelle LF, Carraro L, Cabral M, Vieira A, Coutinho W. An open-label trial of sibutramine in obese patients with binge-eating disorder. J Clin Psychiatry 2002 Jan;63(1): 28-30.

Horvath K, Jeitler K, Siering U, Stich AK, Skipka G, Gratzer TW, Siebenhofer A. Long-term effects of weight-reducing interventions in hypertensive patients: systematic review and meta-analysis. Arch Intern Med. 2008 Mar 24;168(6):571-80.

Saturday, May 31, 2008

Is your cell phone making you fat?


Hmmm...betcha rolled your eyes when you saw THAT headline. So did I until I read this abstract.

Here was the study setup:

Male Djungarian hamsters were exposed, 24 hours a day for 60 days, to radio frequency electromagnetic fields (EMF's) at three different levels of intensity, measured in units of megahertz (MHz). The MHz levels used were the standardized electromagnetic frequency ranges utilized by European telecommunications networks. Exposure equalled the upper exposure limit allowed in Germany.

The hamsters were divided into two groups, one group was actually exposed to the EMF's, while the other was exposed to every aspect of the setup except for the electromagnetic energy. This was to insure that there was not some outside artifact in the setup that might cause any observable change.

At the lowest level of exposure (383 MHz), a temporary increase in body weight up to 4% was observed. At the middle level of exposure (900 MHz), a more significant (up to 6%) and permanent increase was observed. Interestingly, at the highest level of exposure, there were no observable effects on body weight.

What does this mean? Well, the obvious conclusion is that if you are a hamster with weight issues you should stick to using land lines.

Seriously, what I'm drawing attention to here is that sometimes answers to important scientific questions are not always in the most obvious places. A person gains weight, they assume it's about how much they eat and how little they exercise. And, the confounding counterargument is that a person who is spending time on his/her cell phone is not as physically active as someone engaged in other activities. So who's to say what the real cause of the weight gain is?

The other aspect of this argument is the amount of electromagnetic exposure these hamsters were subjected to. It was high, granted, but when I read this study I immediately thought of all the Crackberry...er...make that Blackberry addicts out there, who cannot ever separate themselves from their little electronic gadgets. The people I see at parties, on street corners, etc., who cannot cut the techno-umbilical cord, no matter what interesting and engaging live social opportunity happens to be sitting right in front of them. THAT is the group of people I'd want to study, compared to casual cell phone users...and to...maybe members of that remote South American tribe that just this week had its first-ever introduction to a helicopter.

The connection in this area of research that scientists seem to be pursuing is the effect of electromagnetic activity on the metabolic action of the hormone melatonin. Healthy melatonin function is important for good mental health, and that is what those of you reading this blog are interested in pursuing. And that is why I'm posting this information on this blog. Melatonin is commonly thought of as the sleep hormone, but it has a lot of other very important activities, and its action is sensitive to electromagnetic activity.

There clearly need to be many, many studies that parse this kind of finding into its multiple aspects in order to figure out what exactly is going on. But in the meantime, it's probably not unwise to be sure that you strike a healthy balance when it comes to the amount of time you spend in contact with certain technological toys.

Lerchl A, Krüger H, Niehaus M, Streckert JR, Bitz AK, Hansen V. Effects of mobile phone electromagnetic fields at nonthermal SAR values on melatonin and body weight of Djungarian hamsters (Phodopus sungorus). J Pineal Res. 2008 Apr;44(3):267-72.

Photo courtesy of emotions-concepts.punchstock.com...ain't Google the greatest?