Do you really need fiber to feel full? Do yaaah?

Fiber has long been thought to be essential for satiety, for that full feeling.

It slows digestion, distends the intestine (and I’m not even talking about gas yet) and positively modulates the gut bacteria to promote satiety, or at least that is what the advertisers claim.

There are some studies that show that adding fiber to the diet improves satiety, or at least feeling full (there is a difference there), whereas a multitude of other studies show that fiber has no effect on satiety.

Let me just quote a few snippets:

Snippet 1:

The fibre content of the two breakfasts was: 3 and 12 g of fibre. They found no differences in energy intake at lunch. There was no difference between the diets on desire to eat.


Snippet 2:

Sugar‐beet fibre, which has both soluble (40%) and insoluble (60%) fibres, was used to assess appetite in non‐obese, healthy men and women (Burley et al . 1993a). Four and a half hours after breakfast, participants were provided with an ad libitum lunch. The results showed no significant differences in motivation to eat between the low‐ and high‐fibre breakfasts immediately after breakfast consumption and 4.5 hours later. However, significant differences were observed with energy intakes. After the ingestion of the high‐fibre breakfast, energy, protein and fat intakes were significantly decreased in comparison with the control breakfast.


Snippet 3:

Moderately obese subjects in the treatment group were fed soy crackers, providing 189 kcal and 20.3 g/day of dietary fibre compared with 0.7 g/day of fibre in the placebo cracker. Although there were small changes in bodyweight, hunger ratings on the higher fibre diet were lower at breakfast, although not for lunch and dinner.


Snippet 4:

Viscous fibres may increase satiety. Early trials focused on soluble fibre as the active ingredient in guar gum, pectin and psyllium. Often the insoluble fibre had as much, or more, impact on satiety as the soluble fibre. Many of the more recent trials using soluble fibres that are not viscous, such as RS and inulin, have found no effect on satiety or hunger, even when large amounts of the isolated fibre were fed.


Snippet 5:

During the 4‐week study, subjects consumed their habitual diet plus a daily supplement, comprising either glucose or high‐amylose corn starch (RS2) or extruded and retrograded high‐amylose corn starch (RS3), in a cross‐over, single‐blind, randomised and balanced study design. The dose given was 30 g/day of RS. Consumption of 30 g/day of RS2 and RS3 had little influence on appetite and food intake.


Snippet 6

Neither fiber type nor fiber dose were related to satiety response or food intake.


Snippet 7

Surprisingly, the fibre enrichments studied did not exert effect on appetite sensations and energy intake.


Snippet 8 (from a 15.9 year follow up study):

Our results suggest that greater baseline intake of fruit, but not vegetables or fiber, by middle-aged and older women with a normal BMI at baseline is associated with lower risk of becoming overweight or obese.


It almost feel like I can stop the article right here.

But for those of you who are curious as to what promotes satiety, here we go!

Gut peptides, a fat hormone and cytokine (leptin), a pancreatic hormone (insulin), neurotransmitters (histamine, dopamine and noradrenaline) and neuropeptides are thought to be the main satiety promoting factors.

Neuropeptides and satiety

Neuropeptides involved in satiety, which are secreted from the lateral arcuate nucleus in the hypothalamus, include POMC (proopiomelanocortin) and CART (cocaine- and amphetamine-regulated transcript).

POMC neurons mediate anorexigenic (satiety) responses by the release of alpha-melanocyte-stimulating hormone (α-MSH) which binds to PVN neurons expressing melanocortin-3 and -4 receptors (MC3/MC4-Rs).

NPY (neuropeptide Y) and AgRP (agouti-related protein) are secreted from the medial arcuate nucleus and are involved in hunger.

The orexigenic (apetitic) property of AgRP results from its competition with α-MSH at MC3/MC4-Rs. Among the five subtypes of NPY receptors, NPY-1R, which is expressed on PVN neurons, is primarily responsible for NPY-induced increase in food intake.

The arcuate nucleus receives input from peripheral (brain, pancreas and adipocytes (e.g., leptin, insulin and ghrelin)) and central sources.

In summary, appetite and satiety is regulated by brain neuropeptides, which are regulated by insulin, leptin and ghrelin. Blocking insulin skyrockets hunger so this means that a major cause of hunger is insulin resistance.

Also, leptin has been shown to boost metabolism, reduce appetite, promote fat loss, etc., however, overweight and obese individuals are resistant to the leptin. Research shows that histamine sensitizes the brain to leptin and supplemental histidine (the amino acid precursor to histamine) can reduce hunger and promote fat loss.

Gut peptides and satiety

Furthermore, hunger is thought to be controlled via gut peptides, namely cholecystokinin (CCK), glucagon-like peptide 1 (GLP-1) and peptide YY (PYY). They are secreted from both the proximal and distal intestine in response to the arrival of nutrients into the intestinal tract.

However, how useful are they exactly? According to this study, not so much.

INFUSION studies (with these peptides) showed that minimum increase required to suppress ad libitum energy intake for CCK, GLP-1 and PYY was 3.6-, 4.0- and 3.1-fold, respectively, achieved through DIET in only 29%, 0% and 8% of interventions. Whether circulating ‘thresholds’ of peptide concentration likely required for behavioural change can be achieved through diet is questionable.


So what does it come down to?

The Protocol that Smashes Serotonin and Endotoxin and causes Dopamine to Skyrocket!!!!

This dopaminergic diet is the best thing ever in a highly serotonergic Western environment.

Minimizing insulin spikes by eating low GI?

Nope, there appears to be no difference between low or high GI (R, R). This following paper shows that hunger and satiety hormones balance each other out over time with a low or high GI diet and that there is no difference in hunger.

Thus, it is difficult to conclude that the GI values of foods or mixed meals are a valid long-term predictor for appetite, hunger and satiety. Both insulin and insulin-mediated glucose uptake and metabolism in adipose tissue affect blood leptin concentration and its diurnal pattern. Circulating ghrelin level is suppressed by carbohydrate-rich meals, presumably via glycemia and insulinemia. Accordingly, low-GI foods may not necessarily increase satiety or suppress appetite and/or hunger because of the lack of insulin-mediated leptin stimulation and ghrelin suppression. However, insulin-mediated leptin stimulation and ghrelin suppression per se is not consistent among studies; thus we were not able to identify a clear relationship among GI, satietogenic leptin, and appetitic ghrelin.


Is fat better for satiety than carbs?

Some might think that fat is superior for satiety than carbs, because it slows transit time, lower insulin spikes, etc. Why else would people on keto or carnivore diets have superior satiety and can go long between meals without food?

It turns out to be protein. When protein is equated, a low carb diet wasn’t superior at reducing appetite than a low fat diet.

How important is protein for satiety?

Bodybuilders are well aware of the satiating effect of protein. Protein is not just needed to retain muscle mass during a deficit, but it also helps increases energy expenditure and satiety. Protein is the most satiating macronutrient.

And how does protein enhance satiety? Surprisingly, not through gut peptides, leptin or insulin, but through the availability of amino acids that are not used for protein synthesis (R, R). Fullness might be higher in the high carb diet (due to more volume eaten), but appetite is the same.

For example, despite the satiating effect of dietary protein, which is well supported through dietary studies [48,85], no linear relationship was observed between protein content and GI peptide response in our current review.


And also:

A higher protein diet enhances satiety despite an unchanged leptin and a significantly decreased leptin AUC and increased ghrelin AUC.


And lastly:

The Glucagon-like-peptide-1 (GLP-1) response was smaller following the high-protein lunch, due to the high-carbohydrate induced GLP-1 response during the normal-protein lunch, showing clearly that a GLP-1 response is primarily nutrient related, and only secondarily satiety related


It’s often been thought that it’s the tryptophan content (because serotonin is supposed to be this wonder hormone…it’s not) of the protein that promotes satiety the most. That’s why whey has been shown to be superior than casein at suppressing appetite. But, that was only at low doses of each. Once the doses were increased, there was no difference between whey and casein in terms of appetite suppression.

According to this study, isoleucine, leucine, lysine, methionine, phenylalanine, proline, tyrosine, and valine were significantly inversely correlated with hunger and positively with satiety and GLP-1 (R). Notice tryptophan in not on the list.

I’m going to finish this section with, how much protein is required for a high protein diet. Well most studies compare 12-15% protein with 25-30% protein, which equates to about 144g protein daily on a high protein diet. That’s not even high…at least according to me. That’s like a medium protein diet. A high protein diet is 200g+, which is what I’m consuming daily (which is more suitable/requiered when you have more muscle mass).

Many things can influence satiety, for example, amino acids (in the example of whey, casein, etc. (R, R)), fats, polyphenols, hormones (e.g. histamine and dopamine promote satiety), etc.

What about gut bacteria and short chain fatty acids?

Short-chain fatty acids, either obtained through the diet or created by gut bacteria have been shown to promote satiety, however, the effect on fat loss, glycemia and so on are unclear (R).

But your gut bacteria doesn’t require fiber to create short chain fatty acids. Polyphenols found in fruit juice, lactose in milk, fructose, fructooligosaccharides (found in honey), inulin (found in maple syrup), etc., can also act as prebiotics and promote the production of SCFAs, which in turn can have a favorable effect on appetite.

And it’s important to be careful with excess fiber, as gut bacteria can ferment on fiber and create excess endotoxins, serotonin, histamine, etc. Endotoxins, serotonin and histamine promote inflammation everywhere in the body, reduce insulin sensitivity, promote fat storage in the liver and adipose tissue, cause an immune reaction, damage the testes and lower testosterone production, harm the brain and cause cognitive decline and much more.

So what results in excess hunger?

IMO, inflammation is one of the biggest reasons for excess hunger. Inflammation causes excess lipolysis, insulin resistance and also leptin resistance.

Because of insulin resistance and inflammation, your cells are not getting adequate fuel (example, glucose is wasted to lactate and fatty acids are incompletely oxidized) and thus your body thinks it’s starving.

So to lower excess hunger, it comes down to lowering oxidative stress and inflammation. There are a lot of things (internally and externally) that can cause inflammation, but let’s look at the most important sources of inflammation.

  • Gut issues – leaky gut and pathological gut bacteria
  • Gluten
  • Lectins
  • Excess metals, such as iron, mercury, lead, etc.
  • Accumulation of omega 6 (even if it’s not oxidized or rancid yet). In the 1970s, most people were lean. In the 80s, saturated fat was shunned and vegetable oil exalted by Ancel Keys, et al. Since then, obesity has been skyrocketing. Read more on this in the book “The big fat surprise”.
  • Poor sleep


It might seem like I’m bashing fiber in this article, but I’m just trying to point out that you don’t NEED fiber to feel full. For people that have gut issues/indigestion/bloating/skin disorders, etc., they might benefit from eliminating most fiber-rich foods.

If you don’t react negatively to fiber, then you don’t have to cut it out. But the question you can ask yourself is: “Do I want to improve my health?” The answer is most often yes. If you’re not 100% healthy, your “thermostat” for sensing problematic foods is desensitized and you can’t identify problematic foods properly. So eliminating fiber for a while can be beneficial to see if your health actually improves. Then you can reintroduce foods you crave later on after your inflammation has subsided, to see which foods you react the least negatively to.

As always, thanks so much for reading my article. Let me know in the comments below if you have any questions. And if you found this article to be insightful and helpful please like and share so this information can help others as well.

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