Is feeling hungry bad?

[redrum86]

I am currently in a 500 cal deficit eating clean (steamed broccoli, brown rice, chicken breast, etc..) every 3 or 4 hrs. I just started changing the way I eat as I am fat (25%bf). I feel like I am always hungry, especially at night and sometimes throughout the day. Is this feeling normal? I know I can't eat once I hit my allowance for the day so what do I do? Just deal with it?
My tdee is 2629 and I am currently eating 2129cals a day
im male 28yrs old 6'2 253

[Bio-Active]

Its normal if you aren't hungry then you are probably eating to much

[Docd187123]

You can try eating more very low calorie veggies like lettuce, carrots, etc and increasing your fiber intake will help increase your satiety.

How many times a day do you usually eat?

[kronik420]

I am currently in a 500 cal deficit eating clean (steamed broccoli, brown rice, chicken breast, etc..) every 3 or 4 hrs. I just started changing the way I eat as I am fat (25%bf). I feel like I am always hungry, especially at night and sometimes throughout the day. Is this feeling normal? I know I can't eat once I hit my allowance for the day so what do I do? Just deal with it?
My tdee is 2629 and I am currently eating 2129cals a day
im male 28yrs old 6'2 253

yes it is normal..

you could up the calories and add in more cardio... might work.. or might just make you even more hungry..lol..

[hellomycognomen]

If you are really hungry you can eat and make up for the calories the next day. Just make sure you even out at the end of the week.

It will take a couple of days for body to adjust to the restriction.

You can switch out calorie high foods for lower calorie ones to give you more quantity.

When I used to do restriction I would try and eat smaller in the mornings and during the day so as to have the majority of the calories in the evenings, this worked better for me than trying to space them out evenly.

[Mr. Small]

Usually the first 2 weeks of a diet can be the hardest. Once you get that initiation phase out of the way, you will feel better.
Plate fillers are greens, mushrooms etc.

[jngymrat]

Do you drink any soda's, diet or otherwise? fruit juices, apple, orange, pineapple? any sugar substitutes? How many times a day do you eat and what is a typical daily snapshot of your consumption?

[Matt007]

Diet soda for me bro, some people might argure this but it does no harm hindering your fat loss
If diet pop makes u stop from craving food drink it, if it does the complete opposite, makes u hungry drinking diet pop dont drink it
Diet pop will not hinder fat loss man, drink it all the time shit sometimes 2l a day and still end up loosing 1% bf per week dieting down, at the worsed it has sodium content so u will bloat up abit but the bloat will disapate by morning anyways, goodluck bro

[Chicagotarsier]

Do you have a breakdown of your protien fat carb %s?

Extreme hunger vs hunger hunger is very different. Hunger Hunger can be caused just by stress, or in many circumstances not being hydrated enough. My "thing" is if it is not meal time and i just got to have something I "MUST" drink 1.5L of water (chug it) wait 10 minutes and if still hungry that means I am truly hungry. 9 out of 9 times I am not hungry after the water.

[against_grain]

try adding greens like mentioned above, for example have 2 cups of steamed broccoli with coconut oil (measured to meet your fat intake requirement).

Its a MISSION to eat 2 cups of broccoli but once you do it will help you not be hungry!!

[sgt2jay]

I would stay away from diet soda. I can hinder fat loss. The sweet taste triggers insulin which can keep ya feeling hungry. If you dont already try eating green veggies raw. I get a fuller felling from raw veggies. another trick is dont drink water while eating as well as waiting 30 minutes after, fluids can compress your meal and even push it through quicker. I drink a full cup prior to eating to fill the belly.

[AngryNR3C4]

You miscalculated and should eat more. I'd say somewhere between 2500-3000 cals.
You're most definitely gonna lose a lot of weight on 2500 cals. I wouldn't go lower.

[Docd187123]

I would stay away from diet soda. I can hinder fat loss. The sweet taste triggers insulin which can keep ya feeling hungry. If you dont already try eating green veggies raw. I get a fuller felling from raw veggies. another trick is dont drink water while eating as well as waiting 30 minutes after, fluids can compress your meal and even push it through quicker. I drink a full cup prior to eating to fill the belly.

Sweet tastes trigger insulin? Would you care to expand on that?

[sgt2jay]

SURE - Artificial sweeteners trick the body into thinking it’s consuming real food, and because they’re over a hundred times sweeter than the real thing, your body starts producing insulin (the fat storage hormone). You’re better off consuming the real stuff in moderation

Diet soda not part of athletes diet plan - 9 Foods an Athlete Would Never Eat - Worst Foods for Athletes - Men's Fitness

[Docd187123]

SURE - Artificial sweeteners trick the body into thinking it’s consuming real food, and because they’re over a hundred times sweeter than the real thing, your body starts producing insulin (the fat storage hormone). You’re better off consuming the real stuff in moderation

Diet soda not part of athletes diet plan - 9 Foods an Athlete Would Never Eat - Worst Foods for Athletes - Men's Fitness

Men's fitness is not scientific proof; it is a marketing publication. Here are some actual studies

Aspartame and its constituent amino acids: effects on prolactin, cortisol, growth hormone, insulin, and glucose in normal humans.

AuthorsCarlson HE, et al. Show all Journal
Am J Clin Nutr. 1989 Mar;49(3):427-32.
Affiliation
Abstract
Because large doses of phenylalanine stimulate prolactin secretion in man, we studied the acute effects of oral doses of aspartame (0.534 g, equivalent to the amount of aspartame in approximately 1 L beverage), aspartic acid (0.242 g), and phenylalanine (0.3 and 1.0 g) on serum prolactin and other hormones in normal humans. Prolactin was not stimulated by any of the aspartame meals, aspartic acid, or 0.3 g phenylalanine; a small rise in serum prolactin, similar to that produced by a high-protein mixed meal, followed ingestion of 1.0 g phenylalanine. Serum growth hormone showed no statistically significant changes in response to any of the experimental meals whereas cortisol and insulin fell slightly and glucose rose slightly during each of the meals. We conclude that these doses of aspartame do not alter secretion of prolactin, cortisol, growth hormone, or insulin in normal individuals.

Metabolism. 1990 Apr;39(4):391-6.
Affiliation
Abstract
Seven subjects homozygous for phenylketonuria (PKU) and seven normal subjects were administered four beverage regimens after an overnight fast: unsweetened beverage, beverage providing carbohydrate (CHO), beverage providing aspartame (APM), and beverage providing APM plus CHO. The APM dose (200 mg) was the amount provided in 12 oz of diet beverage; the CHO was partially hydrolyzed starch (60 g). Plasma amino acid concentrations were determined after dosing and the molar plasma phenylalanine (Phe) to large neutral amino acid (LNAA) ratio calculated. APM administration without CHO did not increase plasma Phe concentrations over baseline values in either normal or PKU subjects (5.48 +/- 0.85 and 150 +/- 23.0 mumols/dL, respectively). Similarly, the Phe/LNAA did not increase significantly. Ingestion of beverage providing APM and CHO did not significantly increase plasma Phe concentrations over baseline values in either normal or PKU subjects. However, ingestion of beverage providing CHO (with or without APM) significantly decreased plasma levels of valine, isoleucine, and leucine 1.5 to 4 hours after dosing in both normal and PKU subjects, thereby increasing the Phe/LNAA ratio significantly. These data indicate that changes noted in Phe/LNAA values after ingestion of beverage providing APM plus CHO were due to CHO. The plasma insulin response to beverage providing CHO (with or without APM) was significantly higher in PKU subjects than in normals.

Aspartame: neuropsychologic and neurophysiologic evaluation of acute and chronic effects.

AuthorsSpiers PA, et al. Show all Journal
Am J Clin Nutr. 1998 Sep;68(3):531-7.
Affiliation
Abstract
BACKGROUND: Neurobehavioral symptoms have been reported anecdotally with aspartame.

OBJECTIVE: This study sought to determine whether aspartame can disrupt cognitive, neurophysiologic, or behavioral functioning in normal individuals.

DESIGN: Forty-eight healthy volunteers completed a randomized, double-blind, placebo-controlled, crossover study. The first month was aspartame free. Subjects then consumed sodas and capsules with placebo, aspartame, or sucrose for 20 d each. Order was randomized and subjects were assigned to either a high- (45 mg x kg body wt(-1) x d(-1)) or low- (15 mg x kg body wt(-1) x d(-1)) dose aspartame group. Neuropsychologic and laboratory testing was done on day 10 of each treatment period to determine possible acute effects and on day 20 for possible chronic effects.

RESULTS: Plasma phenylalanine concentrations increased significantly during aspartame treatment. Neuropsychologic results; adverse experiences; amino acid, insulin, and glucose values; and electroencephalograms were compared by sex and by treatment. No significant differences were found for any dependent measure.

CONCLUSION: Large daily doses of aspartame had no effect on neuropsychologic, neurophysiologic, or behavioral functioning in healthy young adults.

An evaluation of the effect of aspartame on weight loss.

AuthorsKanders BS, et al. Show all Journal
Appetite. 1988;11 Suppl 1:73-84.
Affiliation
Abstract
This study explores whether the addition of aspartame-sweetened foods and beverages to a low fat, hypocaloric diet enhances compliance and resulting weight loss. Fifty-nine obese (130-225% of ideal body weight), free living men and women were randomly assigned to either a Balanced Deficit Diet (BDD) or a BDD supplemented with aspartame. Over a 12-week weight loss period, volunteers attended weekly support group meetings including behavior modification training and exercise instruction. Males achieved a clinically significant weight loss (greater than 23 lb) in both study groups, while females lost an average of 12.8 lb in the control group vs. 16.5 lb in the experimental group. In both treatment groups, sleep, general energy level, level of physical activity, and feeling of well-being showed clinically meaningful improvement. This study suggests possible advantages to supplementing a BDD with aspartame-sweetened foods as part of a multidisciplinary weight loss program. The small sample size prohibits definitive conclusions but does provide the protocol for a larger, outpatient clinical trial.

The effect of aspartame as part of a multidisciplinary weight-control program on short- and long-term control of body weight.

AuthorsBlackburn GL, et al. Show all Journal
Am J Clin Nutr. 1997 Feb;65(2):409-18.
Affiliation
Abstract
This study investigated whether the addition of the high-intensity sweetener aspartame to a multidisciplinary weight-control program would improve weight loss and long-term control of body weight. One hundred sixty-three obese women were randomly assigned to consume or to abstain from aspartame-sweetened foods and beverages during 16 wk of a 19-wk weight-reduction program (active weight loss), a 1-y maintenance program, and a 2-y follow-up period. Women in both treatment groups lost approximately 10% of initial body weight (10 kg) during active weight loss. Among women assigned to the aspartame-treatment group, aspartame intake was positively correlated with percentage weight loss during active weight loss (r = 0.32, P < 0.01). During maintenance and follow-up, participants in the aspartame group experienced a 2.6% (2.6 kg) and 4.6% (4.6 kg) regain of initial body weight after 71 and 175 wk, respectively, whereas those in the no-aspartame group gained an average of 5.4% (5.4 kg) and 9.4% (9.4 kg), respectively. The aspartame group lost significantly more weight overall (P = 0.028) and regained significantly less weight during maintenance and follow-up (P = 0.046) than did the no-aspartame group. Percentage weight losses at 71 and 175 wk were also positively correlated with exercise (r = 0.32, P < 0.001; and r = 0.34, P < 0.01, respectively) and self-reported eating control (r = 0.37, P < 0.001; and r = 0.33, P < 0.01, respectively). These data suggest that participation in a multidisciplinary weight-control program that includes aspartame may facilitate the long-term maintenance of reduced body weight.

Now let's assume for a second you may be correct, that artificial sweetners can induce an insulinogenic response although it's a stretch of the facts to say the least, how do you propose a small acute insulin response can counteract a hypocaloric diet? I mean whey protein spikes insulin, do you not use whey for fear of an insulin response?

[sgt2jay]

my only point is if you are hungry and not losing weight and everything else is on point you might want to consider staying away from artificial sweeteners (diet soda). My reference to insulin is probably off point, but if i look hard enough i could probably find just as many studies stating diet soda and artificial sweeteners will hinder weight loss.

[sgt2jay]

I bit more current study

Artificial sweeteners may do more than sweeten: It can affect how the body reacts to glucose -- ScienceDaily

OBJECTIVE Nonnutritive sweeteners (NNS), such as sucralose, have been reported to have metabolic effects in animal models. However, the relevance of these findings to human subjects is not clear. We evaluated the acute effects of sucralose ingestion on the metabolic response to an oral glucose load in obese subjects.

RESEARCH DESIGN AND METHODS Seventeen obese subjects (BMI 42.3 ± 1.6 kg/m2) who did not use NNS and were insulin sensitive (based on a homeostasis model assessment of insulin resistance score ≤2.6) underwent a 5-h modified oral glucose tolerance test on two separate occasions preceded by consuming either sucralose (experimental condition) or water (control condition) 10 min before the glucose load in a randomized crossover design. Indices of β-cell function, insulin sensitivity (SI), and insulin clearance rates were estimated by using minimal models of glucose, insulin, and C-peptide kinetics.

RESULTS Compared with the control condition, sucralose ingestion caused 1) a greater incremental increase in peak plasma glucose concentrations (4.2 ± 0.2 vs. 4.8 ± 0.3 mmol/L; P = 0.03), 2) a 20 ± 8% greater incremental increase in insulin area under the curve (AUC) (P < 0.03), 3) a 22 ± 7% greater peak insulin secretion rate (P < 0.02), 4) a 7 ± 4% decrease in insulin clearance (P = 0.04), and 5) a 23 ± 20% decrease in SI (P = 0.01). There were no significant differences between conditions in active glucagon-like peptide 1, glucose-dependent insulinotropic polypeptide, glucagon incremental AUC, or indices of the sensitivity of the β-cell response to glucose.

CONCLUSIONS These data demonstrate that sucralose affects the glycemic and insulin responses to an oral glucose load in obese people who do not normally consume NNS.

Footnotes

Clinical trial reg. no. NCT01128829, clinicaltrials.gov.
Received October 29, 2012.
Accepted March 5, 2013.

[Docd187123]

That study has little relevance to the discussion at hand. Subjects were taking oral glucose which of course triggers an insulin response. It doesn't show NNS's caused the insulin response which is what had been initially claimed.

If you can find such a study showing a beverage with no calories hinders fat loss in isocaloric diets I'd be very interested in seeing it. As of this time I've yet to see such a study though

[sgt2jay]

Again my point is if one is overweight, diet soda is not a good solution to combating hunger. I will be honest the studies are greek to me and admit that I am probably wrong on my initial point. But the way I read the above study the subject were given sucralose not an oral glucose. The only reference to an oral glucose I see is to the test given. Maybe I am reading it wrong. If one is making progress drinking diet soda then by all means continue, but if you are not I would really take a look at dropping it.

[Docd187123]

Again my point is if one is overweight, diet soda is not a good solution to combating hunger. I will be honest the studies are greek to me and admit that I am probably wrong on my initial point. But the way I read the above study the subject were given sucralose not an oral glucose. The only reference to an oral glucose I see is to the test given. Maybe I am reading it wrong. If one is making progress drinking diet soda then by all means continue, but if you are not I would really take a look at dropping it.

It mentions giving the subjects oral glucose in the objective, design and methods, results, and conclusion.

I can agree that in some people it may stimulate hunger and if that's the case it may be better to drop it. Thank you for expanding on the original comments brother.

[sgt2jay]

ok still more questions - Sorry not trying to start a pissing match here

I am re reading and I still don't see anything that says they were given oral glucose.

I see in the objective - sucralose ingestion and
The Design and Method - modified oral glucose tolerance test on two separate occasions preceded by consuming either sucralose or water
The Results - sucralose ingestion
The Conclusion - sucralose

I do see where they talks about the oral glucose load but I read that as the bodies response to sucralose which is why the had to the modify oral glucose tolerance test.

thoughts?

[Docd187123]

ok still more questions - Sorry not trying to start a pissing match here

I am re reading and I still don't see anything that says they were given oral glucose.

I see in the objective - sucralose ingestion and
The Design and Method - modified oral glucose tolerance test on two separate occasions preceded by consuming either sucralose or water
The Results - sucralose ingestion
The Conclusion - sucralose

I do see where they talks about the oral glucose load but I read that as the bodies response to sucralose which is why the had to the modify oral glucose tolerance test.

thoughts?

Not at all, I don't think you're starting anything. This is what it says in the conclusion for example:

CONCLUSIONS These data demonstrate that sucralose affects the glycemic and insulin responses to an oral glucose load in obese people who do not normally consume NNS.

[thisAngelBites]

The cephalic phase response (that the taste, smell, even some thoughts of food itself) causes insulin production. Google it.

I experiment on myself a fair amount, and I can also tell you empirically that drinking black decaf coffee with stevia in it lowers my blood glucose. Camomile tea with stevia in it lowers my blood glucose. I have tested these scenarios more than 50 times. Non caloric beverages with sweetener definitely lower my BG. I take that to be a good thing, but I don't know the limits of the cephalic response and how much insulin is secreted, and whether (wrt to artificial sweeteners) it is dose-dependent. I've never tried drinking a lot of coffee with stevia to see whether I could make myself slightly hypoglycemic and therefore hungry. Although now that I am speaking about it, I'd say that I usually want breakfast fairly soon after a black coffee with stevia, and can wait almost until lunch if I have a latte instead. And maybe that's the result of the differences in BG. I guess I need another experiment to see.

[Docd187123]

Thank you for chiming in with your thoughts Angel. I did a little research on the cephalic response and found mixed opinions on it. The quote by Ross has the figures of the insulin response you had questioned .

Here are some of the quotes I've been looking at:

The insulin response would be very transient anyway, and not have any impact on the end result. For some, drinking/eating something with sweeteners makes them crave more, for some it makes the diet more tolerable - so find out what applies to you and go with that.

sweet tastes per se, in some people can generate a cephalic insulin response, it's nothing to do with the inertness or not per se.

this has been discussed here before

but it doesn't matter beyond what Blade wrote: for some sweet tastes makes them crave more sweet and this can derail a diet, for others it makes the diet survivable b/c they can fix sweet cravings with somethign non-caloric

if you get on pubmed, make sure to look at more than one paper since the insulin response to artificial sweeteners tends to show up in some studies but not others so it's easy ot draw weird conclusions. in general, as I recall, it was type II diabetics or pre-diabetics who had the most pronounced response. but they release insulin to just about anything

Section I. “All Sweeteners Can Contribute to Weight Gain or Prohibit Weight Loss”

Sanfilippo’s first section contends that all sweeteners, including non-nutritive sweeteners, can contribute to weight gain or stymie weight loss. Her argument relies heavily on the idea that cephalic phase insulin response (insulin released by the pancreas in response to the taste of sweet food) causes fat storage, even if the sweet tasting food was non-nutritive. As she sums it up, “Eat something sweet (regardless of calories) > Insulin is released > Body stores nutrients.”

Sanfilippo encourages her readers to use their independent judgment, rather than “[taking] her word for it,” and, to this end, she supplies three sources (2 of which are peer-reviewed) which she says support her argument.

The problem is that these sources don’t support her argument very well. The first source[i] (chronologically) is a 1987 paper that examines the effect of acesulfame potassium injection/infusion on peripheral plasma insulin levels in rats. In other words, this study doesn’t even look at cephalic phase insulin secretion at all—rather, it looks at the effect of artificial sweetener in the blood (not in the mouth) on insulin secretion. While this might also be an interesting thing to study, the results aren’t too exciting in my opinion. The researchers achieve increased insulin levels after injection of 100 mg/kg-bw (milligrams per kilogram of body weight) but not at lower levels. I wasn’t able to find how much acesulfame-K is in a typical diet soft drink, but it has similar sweetness to aspartame, which is usually present in about 180 mg per 12-ounce can of soft drink. Assuming similar physiology between a human and a rat (which is not always a valid assumption) this study suggests that increasing insulin secretion in the average 70 kg male would require injection of 7g (7000 mg) of acesulfame-K, which is the equivalent of ~39 diet soft drinks. The infusion data used similarly inflated amounts of artificial sweetener to evoke increased plasma insulin concentrations. And, perhaps least impressively, the researchers were able to evoke the same responses with equal mass infusions of glucose (sugar). Given that most diet soft drinks have 27-30g of sugar and 180 mg of acesulfame/aspartame, it doesn’t raise my eyebrows too much to see that 180 mg of acesulfame-K might raise my insulin by as much as 180 mg (0.18g) of sugar. That's not that much sugar.

There are numerous sources available that use grossly inflated masses of artificial sweeteners to evoke some negative effect in an animal (e.g., rat, mouse) that are then used in attempts to prove that artificial sweeteners are harmful to human beings. I’m not convinced by these, because dose determines the poison, and few if any of these studies are able to produce negative effects with masses of artificial sweetener that actually mimic that seen in typical human consumption.

There are some sources that suggest that artificial sweeteners can produce a cephalic-phase insulin response, but these are also not particularly impressive to me. The cephalic phase insulin response shown in these studies has been routinely shown to be brief, lasting only minutes, with a range of increase in plasma insulin between 7-75% in humans and 200% in rats. Compare this to the average insulin increase from digesting a nutritive meal (500-1200% increase). Given the body of research I have read, I’m not convinced that the taste of sweeteners contributes to obesity through causing insulin release. [I am open to the idea that it might contribute by other mechanisms, and I think Stephan Guyenet's posts on the food reward hypothesis of obesity to be both interesting and compelling]

Sanfilippo’s second source is a news article from MedScape that reports that an association has been found between aritificial sweeteners and Type-II diabetes mellitus. Reading the article, however, confirms that this study is only associational and the results can easily be explained by the strong possibility that obese, type-II diabetics are more likely to use artificial sweeteners, perhaps in attempts to lose weight.

Sanfillipo’s third source[ii] is a psychological study examining the role of sweet taste in energy balance. It’s actually pretty interesting. The authors hypothesized that sweet-taste indicates caloric content to the brain, and that when sweet taste is decoupled from caloric content, as in foods sweetened with non-nutritive sweeteners, the body responds by increasing caloric intake. The research was done in rats, which is a weakness when you’re trying to draw a nutritional conclusion for human beings. Most importantly though, the source is not, as Sanfilippo suggests, an examination of the role of artificial-sweetener-induced insulin-release (particularly CPIR) in weight gain.

Sanfilippo goes on in this section of her post to provide a whole list of symptoms/problems that are allegedly caused by artificial sweeteners. My thoughts are that, while artificial sweeteners may truly cause these symptoms in some individuals, I am not aware of any evidence suggesting that these effects are widespread (e.g, convulsions/seizures from diet soda). Sanfilippo gives this list as evidence that everyone, even those who are not overweight, will benefit from removing artificial sweeteners from his/her diet. To me, this list just suggests that someone experiencing one of the listed symptoms should experiment by removing sweeteners for a period of time (1-6 months), and see if the symptoms return on re-introduction of the sweeteners. She doesn’t make a very strong case for removal of these agents for people who have healthy weight and no medical problems.

New Study Demonstrates that Sugar has to be Palatable to be Fattening in Mice
Dr. Anthony Sclafani's research group just published a study definitively demonstrating that high palatability, or pleasantness of taste, is required for sugar to be fattening in mice (1). Dr. John Glendinning was lead author. Dr. Sclafani's group has done a lot of excellent research over the years. Among other things, he's the person who invented the most fattening rodent diet in the world-- the 'cafeteria diet'-- composed of human junk food.

Mice and rats love sweet food and drinks, just like humans. If you give them a choice between plain water and sugar water, they'll overconsume the sugar water and become obese. I have argued, based on a large body of evidence, that the reward value and palatability* of these solutions are important to this process (2, 3, 4). This is really just common sense honestly, because by definition if the solution weren't rewarding the mice wouldn't go out of their way to drink it instead of water, the same way people wouldn't go out of their way to get soda if it weren't rewarding. But it's always best to confirm common sense with research.

This study didn't address reward in any case-- it was focused specifically on palatability. In mice as in humans, sweet tastes are detected by special proteins on the tastebuds, and the signal is transmitted within the cell by another set of proteins, and the genes encoding these proteins are known. Dr. Sclafani's group asked a simple question: "is sugar still able to make mice obese if they can't taste its sweetness?" They did this by genetically "knocking out" two different proteins, one in each line of mice, that are required for the perception of sweetness on the tongue (5).

The investigators showed that mice lacking these proteins have a normal food intake and body fatness when fed standard lab chow, but unlike normal mice both mutant strains are almost completely resistant to fat gain when given a sugar solution. This is despite the fact that they drank a similar amount of sugar as the normal mice, which became obese**. Basically, they drank the sugar water but it was no longer fattening once it didn't taste sweet.

But here's the coup de grace. To make sure the mice weren't just resistant to obesity in general for some reason that has nothing to do with palatability, they altered the sugar solutions by adding a very small amount of fat emulsion, so that the solutions were once again palatable to all groups of mice. Now, suddenly, the mice that couldn't taste sweetness got just as fat on the sugar solution as normal mice! The paper's main conclusion:
Our results suggest that nutritive solutions must be highly palatable to cause carbohydrate-induced obesity in mice...
I couldn't imagine a better way to test this hypothesis, and even I wouldn't have expected such a striking outcome. This study completely shuts down the argument-- never convincing to begin with-- that food palatability is not relevant to body fatness. Consistent with a large body of evidence in animals and humans, it supports the prevailing view among obesity researchers that excessive food palatability is an important factor in the development of obesity. It also supports the argument I made in my post "Is Sugar Fattening?", that added sugar can be fattening because it increases the energy density, palatability, and reward value of food, rather than due to a metabolic effect that occurs after ingestion.


* Reward. The brain contains a "reward" system, whose job it is to gauge the desirability of food (among other things) and reinforce and motivate behaviors that favor the acquisition of desirable food. For example, if you eat a strong cheese for the first time, maybe it won't taste very good to you. As it's digested, your reward system gets wind that it's full of calories however, and the next few times you eat it, it tastes better and better until you like the flavor. This is called an acquired taste, and the reward system is what does the acquiring, motivating you to obtain a food it has deemed safe and desirable. Eventually, you may go out of your way to purchase the cheese or beer at the grocery store because you like it so much, and maybe you'll consume cheese or beer even if you aren't hungry or thirsty. This is an example of the reward system reinforcing and motivating behaviors related to foods that it considers desirable. Processed "junk foods" such as ice cream, fast food, sweetened soda, cookies, cake, candy and deep fried foods are all archetypal hyper-rewarding foods.

Palatability is a related concept-- it is simply the pleasantness of a food; how much a person enjoys eating it. Palatability is determined in part by inborn preferences (e.g., a taste for sugar and energy dense foods), and in part by the reward system (acquired tastes). Palatability is governed by the hedonic system in the brain, which is closely integrated with the reward system.

The reward system is what motivates you to get food and put it to your lips, every time you eat. When scientists shut it down in mice, they completely cease eating (6). The hedonic system influences how much you eat once you begin a meal-- highly palatable food generally increases food intake by activating this system (7). Together, reward and hedonic circuitry in the brain determine in large part how often you eat, what you eat, and how much you eat, and this is influenced by the attributes of the food that's available.

** Basically, they still find the sugar solution rewarding, just not palatable. It has been known for a while that sugar receptor knockout mice still find sugar rewarding. It just takes them longer to develop that reward association, as Dr. Sclafani's paper demonstrated. The post-ingestive effects of the sugar allow them to form a conditioned preference for the sugar bottle, and therefore seek it out and drink a bunch of it, despite the fact that it doesn't taste sweet to them.

From the above and other pages I've looked at it seems to me that the cephalic response in humans is still not conclusive. Some studies have shown a clear physiological response while others haven't. According to Lyle McDonald, he believes it's Type II diabetics and pre-diabetics who had the most pronounced response and even in those who did have a response, it was transient and has not been shown to have clinical significance from what I can tell. I've not seen any reference to where this cephalic response stalled fat loss as well, maybe you have?

The cephalic response does somewhat tie in to Stephen Guyenet's Food-Reward hypothesis on obesity which I find to be a very compelling argument.


Sgt2Jay, it looks like I was too quick to brush off your idea of an An insulin repsonse from NNS. I apologize for my haste yet I stand by my comments that any inhibition of fat loss from this phenomenon is psychological and not due to any metabolic differences. Thank you for bringing this to my attention .

[hellomycognomen]

Docd you are a research machine!

-Cheers

[sgt2jay]

Sgt2Jay, it looks like I was too quick to brush off your idea of an An insulin repsonse from NNS. I apologize for my haste yet I stand by my comments that any inhibition of fat loss from this phenomenon is psychological and not due to any metabolic differences. Thank you for bringing this to my attention .

It was just something I found. One other thing I think is key and how it relates to this post is this was a study of obese subjects. Maybe the response to NNS is different or greater (meaning a measurable difference) in the obese as opposed to someone in better physical condition

[thisAngelBites]

I haven't yet had a chance to read all the quotes but I will - thanks for posting them. It's good when we all learn something. But I will point out that I am not a type 2 diabetic (I have a typical fasting blood glucose of about 75) and am not obese, and I see the effect. I wouldn't be surprised if the effect is transient, but even a bit of a drop can be enough to stimulate hunger. I am going to play around with it and see if I can learn something about the hunger effect for my own=1.

[Docd187123]

It was just something I found. One other thing I think is key and how it relates to this post is this was a study of obese subjects. Maybe the response to NNS is different or greater (meaning a measurable difference) in the obese as opposed to someone in better physical condition

Lyle mentioned the greatest effects were seen in type II diabetics and pre-diabetics. While these conditions don't necessarily mean obese or vice versa I would guess this would have some effect on the results yes.

I haven't yet had a chance to read all the quotes but I will - thanks for posting them. It's good when we all learn something. But I will point out that I am not a type 2 diabetic (I have a typical fasting blood glucose of about 75) and am not obese, and I see the effect. I wouldn't be surprised if the effect is transient, but even a bit of a drop can be enough to stimulate hunger. I am going to play around with it and see if I can learn something about the hunger effect for my own=1.

My sister is diabetic and relies heavily in stevia and other NNS I will ask her if she too has noticed any effects on fasting glucose levels.

I guess the hunger part is what Sgt2jay had been talking about which I can agree with. I was arguing something else mainly which is that even with this insulin response, it doesn't physiologically prohibit fat loss.

Let us know what your results are from your experiments!

[redrum86]

Sorry guys I was on vacation and couldn't answer.
I wanted to thank EVERYONE for chiming in. Much appreciated.

You can try eating more very low calorie veggies like lettuce, carrots, etc and increasing your fiber intake will help increase your satiety.

How many times a day do you usually eat?

I am already doing that. I even take a fiber supplement to add extra fiber to my diet as well as making me go regular.
I eat about 5 times a day. I wake up at 0430 and am in bed by 2200. Its a long day so its hard to stay full.

Do you drink any soda's, diet or otherwise? fruit juices, apple, orange, pineapple? any sugar substitutes? How many times a day do you eat and what is a typical daily snapshot of your consumption?

The only thing I drink is water. I eat about 5 times a day. I try to have about 225g of protein, about 135g of carbs and 85g of fats. I always go over on my carbs and a little under on my fats. I am still trying to get a hang of this nutrition thing.

You miscalculated and should eat more. I'd say somewhere between 2500-3000 cals.
You're most definitely gonna lose a lot of weight on 2500 cals. I wouldn't go lower.

I was sedentary and my tdee was 2630. Minus 500 cal deficit and thats my 2130. Verrified off of roughly 4 different sites using different calculations and also doing it manually

[infinite_loop]

There's allot of reasons you could feel hungry. One is that your body is not producing enough leptin for various reasons, another is that rice spiked your insulin too high, causing hypoglycemia and low blood sugar, another is that it wasn't enough cals... However when cutting, hunger is a side effect.