Yep I'm pretty sure that's what it is.

If I don't take my meds (which completely blunts my appetite) I want to eat anything and everything all day. I even find myself eating when I'm not, or shouldn't be feeling hungry. It's as if there's no 'full' switch.

From what I understand people with narcolepsy lack the ability to produce the hypocretin (a.k.a orexin) peptide which is responsible for maintaining appetite and the way the body uses energy.

I hope that's correct, there's a number of other people on here that know a great deal more than me so hopefully they can explain in more detail :)

I'm the same way... on meds, I hardly eat. Off meds, I eat forever.

I think it's because I need energy and my body thinks that's where to get it.

It may also be the control center for appetite, like Andrew said.

thats like me i thought i was addicted to food. I wonder if the doc can give any thing to help. cos my weight is far too much.

when i was diagnosed i was told to cut down on the carbs, i was fine to have caffine but not in chocolate form, they also mentioned a conection between narcolepsy and sleep apnea when we are over weight.

My appetite plummets to zero while on meds, but off them I tend to eat all day. But after sleeping for so long, it doesn't surprise me that I'm hungry! I'm actually technically underweight though.

This is one article on N and eating that Andrew alerted us too a while ago.
http://www.sciencedaily.com/releases/2008/03/080301214742.htm

Thank you so much every1. I thought it was something i was doing wrong. wonder if you can get anything from the doc to help this?

Here's some scientific "food for thought." This study is right on point for this discussion, so I'll post the abstract in its entirety
(skim to the "RESULTS" for the punch line):

Sleep. 2007 Oct 1;30(10):1267-73.
Eating disorder and metabolism in narcoleptic patients.
Chabas D, Foulon C, Gonzalez J, Nasr M, Lyon-Caen O, Willer JC, Derenne JP, Arnulf I.

"STUDY OBJECTIVE: To evaluate eating behavior and energy balance as a cause of increased body mass index (BMI) in narcolepsy...."

"PARTICIPANTS: 13 patients with narcolepsy (7 "typical" patients, with HLA DQB1*0602 and clear cut cataplexy, with suspected hypocretin deficiency; and 6 "atypical" narcoleptics, i.e., HLA negative or without cataplexy), and 9 healthy controls matched for age, gender, and ethnicity.

INTERVENTION: Energy balance was evaluated by measuring BMI, rest energy expenditure with calorimetry, daily food and water intake, and plasma hormone levels. Eating behavior was evaluated using psychometric tests (EAT-40, EDI2, CIDI-2, MADRS).

RESULTS: Patients with narcolepsy (whether typical or not) tended to be overweight and to have a lower basal metabolism than controls. Only patients with typical narcolepsy tended to eat less than controls. Narcoleptic patients who were overweight ate half as much as others, indicating caloric restriction. Plasma glucose, cortisol, thyroid, and sex hormones levels did not differ between groups, while prolactin levels were twice as high in patients with narcolepsy as in controls. Narcoleptic patients had higher EAT-40 scores and more frequent features of bulimia nervosa (independent of depressive mood) than controls, suggesting a mild eating disorder, classified as "Eating Disorder Not Other Specified."

DISCUSSION: Both lower basal metabolism and subtle changes in eating behavior (rather than in calorie intake) could explain the positive energy balance leading to overweight in narcolepsy. Eating behavior changes may be a strategy to control weight or to avoid daytime sleepiness."

Following that study....:

Sleep. 2008 Mar 1;31(3):335-41.
High prevalence of eating disorders in narcolepsy with cataplexy: a case-control study.
Fortuyn HA, Swinkels S, Buitelaar J, Renier WO, Furer JW, Rijnders CA, Hodiamont PP, Overeem S.
Department of Psychiatry, Radboud University Nijmegen Medical Center, Nijmegen, The Netherlands. H.Droogleever-

"STUDY OBJECTIVES: To study the prevalence of and symptoms of eating disorders in patients with narcolepsy.

DESIGN: We performed a case-control study comparing symptoms of eating disorders in patients with narcolepsy versus healthy population controls, using the Schedules for Clinical Assessment in Neuropsychiatry (SCAN 2.1). To study whether an increased body mass index (BMI) could be responsible for symptoms of an eating disorder, we also compared patients with BMI-matched controls, using the SCAN as well as the Eating Disorder Examination-Questionnaire.

PATIENTS AND PARTICIPANTS: Patients with narcolepsy/cataplexy (n = 60) were recruited from specialized sleep centers. Healthy controls (n = 120) were drawn from a population study previously performed in the Netherlands. Separately, 32 BMI-matched controls were recruited.

MEASUREMENTS AND RESULTS: In total, 23.3% of the patients fulfilled the criteria for a clinical eating disorder, as opposed to none of the control subjects. Most of these were classified as Eating Disorder-Not Otherwise Specified, with an incomplete form of binge eating disorder. On the symptom level, half of the patients reported a persistent craving for food, as well as binge eating. Twenty-five percent of patients even reported binging twice a week or more often. When compared with BMI-matched controls, the significant increases persisted in symptoms of eating disorders among patients with narcolepsy. Except for a higher level of interference in daily activities due to eating problems in patients using antidepressants, medication use did not influence our findings.

CONCLUSIONS: The majority of patients with narcolepsy experience a number of symptoms of eating disorders, with an irresistible craving for food and binge eating as the most prominent features. Eating disorder symptomatology interfered with daily activities. These findings justify more attention for eating disorders in the treatment of patients with narcolepsy."

A more recent study (I cut out most of it) found some difference in the basal metabolic rate of non-obese narcoleptics, but that once they're obese, their BMR is no different than obese people without narcolepsy:

Sleep. 2009 Jul 1;32(7):962-4.
Basal metabolic rate in narcoleptic patients.
Dahmen N, Tonn P, Messroghli L, Ghezel-Ahmadi D, Engel A.

This study investigated basal metabolic rate (BMR) and energy expenditure (EE) in narcoleptic patients versus BMI-matched people without narcolepsy. "Our study suggests that energy expenditure plays a role in narcolepsy associated obesity. We propose that narcolepsy may lead to a shift of individual BMI set points."

They further summarized the prevailing theory. First, they pointed out that the leading hypothesis about N is that it is an auto-immune disease, or otherwise (in some way) damages hypocretin-containing cells in the hypothalamus. They also highlighted that other studies have found that tumors or direct damage to the hypothalamus has been found to lead to something called "hypothalamic obesity" (HO), and that it was a change in energy expenditure rather than energy intake (i.e., they were gaining weight because they were burning less calories than normal rather than simply eating more). "In addition narcoleptic patients as well as orexin deficient narcoleptic mice eat less than controls, and actigraphic studies have so far failed to show a general reduction of physical activity of narcoleptics." So, the theory is that their metabolic rate is slower, rather than being dramatically less active or eating more.

They do believe that orexin/hypocretin causes decreased appetite, increased metabolism and increased activity. So, if you have a deficiency of orexin/hypocretin.... Now, the 2009 study above said that they had too few patients to differentiate between narcoleptics that had measured orexin/hypocretin deficiencies (this is tested in a CSF sample), but that nevertheless, "it is known that both orexin-deficient and orexin-non-deficient narcoleptic patients show increased BMIs." I'm guessing that people with N who have adequate hypocretin could have something else "broken" in the system or pathway. I.e., the receptor for hypocretin has mutated or is off, or there is something else binding to the receptor that blocks the hypocretin, or the hypocretin they produce is a little different in shape (enough so it doesn't work, but not enough that the test for hypocretin in CSF doesn't identify it).

Anyway, feel free to ignore this if it's too much science. And remember that research is just that - not completely hard fact yet or 100% proven. But for anyone curious, that's some of the more recent research on the topic (i.e., it's not just imagination - narcolepsy, metabolism, carb cravings and weight gain ARE related).

And sorry for not editing more out - it's hard to do that in this little window, and I'm.....errrrrr.....doing several things at once (I'm in class - sorry!, and our topic today is actually appetite, metabolism and body composition!).

pameladunbar: Are you on any medications for narcolepsy? Many of them decrease appetite (as a side effect). Especially the stimulants and xyrem. Some anti-depressants, on the other hand (which may be prescribed for cataplexy) may have the opposite effect and/or cause someone to gain weight.

yeah i take chlomipramine and modafinil when i first took them appetitie was really low but only for a week or two now just as bad again lol.

Awesome stuff Nyxx, thanks!!

Andrew: Whew! I was scared I was going to get booted off the site for that post!

Pam: Here's another paper that I think you'll find interesting if you were wondering about chlomipramine research:

Biol Pharm Bull. 2007 Aug;30(8):1541-6.
Effect of chronic treatment with clomipramine on food intake, macronutrient selection and body weight gain in rats.

Calegari L, Gorenstein C, Gentil V, Planeta CS, Nunes-de-Souza RL. Laboratory of Pharmacology, School of Pharmaceutical Sciences, So Paulo State University, 14801-902 Araraquara, SP, Brazil.

"Long-term treatment with clomipramine (CMI), a tricyclic antidepressant, induces food craving and body weight gain in patients. The present study investigated the effects of chronic treatment with CMI on total food intake, macronutrient selection, and body weight gain in rats. Male Wistar rats were maintained on a dietary self-selection regime with separate sources of protein, fat and carbohydrate. Animals received i.p. injections of CMI (0, 3, 10, 30 mg/kg) during 27 consecutive days. Food consumption and body weight were recorded daily and results were calculated as average of three consecutive days, namely during pre-treatment (3 d before pharmacological treatment), treatment (7th-9th; 16th-18th and 25th-27th days), and post-treatment (28th-33rd days).

Results showed that CMI (30 mg/kg) significantly decreased energy intake during all treatment period, an effect that was related to a decrease in both carbohydrate-rich diet intake and body weight gain. At dose of 3 mg/kg CMI increased the total energy intake in the 16th-18th days, suggesting an apparent biphasic effect of chronic treatment with CMI on caloric intake. Chronic administration with CMI (27 d) did not alter protein-rich or fat-rich diet consumption. The main result of this study indicated that chronic treatment with CMI decreases rather than increase food consumption and body weight gain in rats exposed to a macronutrient self-selection procedure."

It found that CMI didn't increase food consumption or weight gain in rats BUT they did acknowledge that in clinical settings HUMAN patients complain of both. Here is their discussion of the limitations of the study and the clinical reality observed in practice:

"Although it has been shown that acute injections of CMI
increase carbohydrate intake most studies concerning long term administration of TCA have shown either no changes or
a reduction of food and carbohydrate intake. Indeed, a more
detailed analysis showing the effects of desmethylimipramine
on food intake has revealed that this TCA initially reduces
food consumption, but losses its effects over a long-term
treatment with animals returning food intake towards
pretreatment levels. Nobrega and Coscina showed that
despite manipulations such as drug dosage, route and regime
of administration, diet composition and palatability, animal
gender and housing conditions, chronic treatments with TCA
did not increase food intake or rates of weight gain in rats.
The food intake reduction and weight loss observed in CMI treated
animals may be related to the selectivity of this TCA
in blocking serotonin reuptake. In fact, selective serotonin
reuptake inhibitors were thought to induce weight loss rather
than weight gain in patients without psychiatric disorders.
Thereafter, it is relevant to identify the mechanisms by which
CMI decrease food intake and body weight. However, it must
be emphasized that CMI effects on body weight and food
consumption observed in the present study were obtained
only with the highest dose (30 mg/kg). At 30 mg/kg/d, CMI
may be toxic for rats. Thus, both reductions on food intake
and body weight are likely related to the drug toxicity. The
recovery in total energy intake observed after drug treatment
period (see Fig. 2; group CMI-30 mg/kg) seems to corroborate
this hypothesis.

In conclusion, the use of macronutrient self-selection protocol
in this study provided results that corroborate previous
findings demonstrating that chronic treatment with TCA does
not increase food consumption and body weight gain in
experimental animals. It has been demonstrated that
chronic treatment with tricyclic antidepressants elicit brain
monoamine receptor adaptations. However, present results suggest these possible neurochemical changes neither
influence food consumption nor body weight gain. In addition,
the present results do not support clinical findings,
which have indicated that long-term treatment with TCA can
induce body weight gain and carbohydrate craving in a significant
proportion of patients. Further studies, particularly
those resembling human regimen of macronutrient intake,
should be designed to examine the mechanisms by which
TCA like CMI affects macronutrient consumption. Moreover,
besides affecting serotonergic and noradrenergic neurotransmissions CMI also binds to other receptors such as H1
and muscarinic receptors. Thus it is also relevant to investigate
the mechanisms by which this TCA affects food consumption."

So, they do at least acknowledge weight gain and carbohydrate craving in "a significant proportion of patients." Add to that the supposed metabolism and weight gain problems of narcolepsy, and it's not a pretty scenario.

Regarding weight loss from stimulants, I've read that some people lose weight on provigil, while others don't. Commonly, there is some weight loss for a few weeks, but then things stabilize or go back to where they were before. Switching to a different stimulant might help (if your doctor is willing to prescribe something else - I've heard some general practitioners are nervous about prescribing stimulants other than provigil/nuvigil because of the risk of abuse (which studies have shown is ridiculously low in narcoleptics).

I wish I knew why I cant loose weight. I dont eat much and mostly am never hungry. I do know now after having kidney stones that I need to watch my salt intake. I am now trying to make a positive effert in eating healthier. One thing I do wish is that there were a list of name brand foods that are healthier to eat. There are all kinds of things that tell you the kind of food you should eat but I sit in the store isles for hours trying to read labels and the lights get to me and cause attacks.

Any suggestions on items that are good?

Thats wierd nyxx cos the foods i crave are high carbs bread pasta and crisps mainly quite often potatoes wierd. Thanx.
Wish i had an answer RenatrFr! x

I've always suspected a relation between the two...I've gone off my meds for long periods of time, and whenever I'm off...i turn into a bottomless pit. Even at the end of the day, when my meds are wore off...I can eat till it hurts, but my brain is never full. No one understands what I mean by, physically full, but still hungry...I have eaten an entire pizza, then munched on some chips & salsa, then some ice cream, then milk and cookies.....and then halloween candies, then sneak into the kids chrismas candy,lol. You get the point...
But when I'm on my meds, I eat normally. I can still eat a lot, I just feel "full", mentally and physically. And have control on snacking and cravings. I take adderall and dexedrine. When I was a teenager It took a while for my body to get used to ritalin, and for a while I didn't have much of an appitite, but that all regulated it's self, but the ritalin always gave me a upset stomach. so far what Im taking now works best for my N, and the appetite thing.