Lean protein and satiety -
Choose the most healthful sources of protein. Good protein-rich foods include fish, poultry, eggs, beans, legumes, nuts, tofu, and low-fat or non-fat dairy products.
These three strategies fit in with the Mediterranean and Dietary Approaches to Stop Hypertension DASH diets. The DASH diet includes 2 or fewer servings of protein per day, mostly poultry or fish. Heidi Godman , Executive Editor, Harvard Health Letter. As a service to our readers, Harvard Health Publishing provides access to our library of archived content.
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To answer this, we should look at why high protein intakes may be appetite suppressing in the first place. In the gut, amino acids stimulate the release of several hormones that activate satiety centers in the brain, namely glucose-dependent insulinotropic polypeptide GIP and glucagon-like peptide-1 GLP However, the theory breaks down on all 3 levels in several studies.
High protein meals do not always stimulate more appetite-mediating hormone release or suppression than high carb or high fat meals.
On the flip side, different meals with the same macros can result in major differences in gut hormone production. Higher protein intakes also do not always result in greater appetite suppressing hormone levels nor lower hunger hormone levels than lower protein meals, even when the high protein meals have a higher total energy content [ 3 ].
The response of gut hormone levels to protein also seems to depend on whether someone is lean or overweight. Other researchers propose that large neutral amino acids LNAAs that can cross the blood-brain barrier directly alter brain activation and neurotransmitter levels with appetite suppressing effects.
However, Koren et al. In conclusion, the evidence for direct hunger controlling mechanisms of protein is just as inconsistent as the evidence for the actual appetite suppression. Put simply, protein leverage theory states that the body monitors protein consumption to ensure we consume enough of it.
Specifically, our appetite stays up until protein requirements have been met. The exact mechanisms are still being uncovered, but research indicates a link between satiety signaling in the brain and amino acid utilization in our body.
Activation of anabolic signaling pathways mTOR and suppression of catabolic signaling pathways AMPK reduce food intake by acting on the hypothalamus.
A key modulator in the brain may be GCN2 general control nonderepressible 2 , which quite directly monitors amino acid balance and thereby basically the protein quality of our diet.
We also have receptors in our mouth that detect amino acids. In rodents and several other animals, including pigs, protein leverage theory has strong supporting evidence. After protein deprivation, when given the choice between high and low protein food, they tend to prefer the higher protein food.
Rats can even self-select foods with complementary amino acid profiles. This preference for higher protein foods to meet bodily demands occurs independently of energy balance.
Protein seeking correlates surprisingly well with protein needs for muscle growth in animals. Birds bred to have more muscle also select higher protein diets and male birds eat more protein than female birds. It should be noted the ability of animals to leverage protein is limited and some research finds protein intake has no effect on energy intake at all.
However, the research we have is promising. We also have a low drive to eat protein sources with an incomplete amino acid profile lacking in essential amino acids , as we cannot meet protein requirements with those foods. These phenomena are impossible to explain with the simple model that protein is inherently more satiating than carbs or fats because it directly stimulates satiety hormones.
The satiating effect of high protein meals decreases after high protein diets and comes back after low protein intakes. In other words, if you consume a diet higher in protein than you need, protein will lose some of its satiating effect. The body can sense excess protein intake in the form of increased protein oxidation rates.
Otherwise high protein environments would cause us to starve ourselves. To the best of our knowledge, Holt et al. In their study, they rated satiety for 38 foods, and protein-rich food received the highest ratings, followed by carbohydrate-rich and fat-rich foods.
One of the important mechanisms of HPD-induced satiety involves elevation of the anorexigenic hormones glucagon-like peptide- 1 GLP-1 , cholecystokinin CCK , and peptide tyrosine-tyrosine PYY. These cells detect nutrients in the gastrointestinal tract and release GLP-1, PYY, and CCK, which increase satiety and decrease food intake.
Ghrelin is an orexigenic hormone that induces food intake by increasing hunger, and its plasma concentration is decreased by protein intake. In conclusion, dietary protein elevates GLP-1, CCK, and PYY levels, which are secreted in the gut and diminish appetite while also decreasing ghrelin levels, which increases appetite.
Such changes in the release of satiety hormones constitute an important mechanism of HPD-induced weight loss. The aminostatic hypothesis, which proposes that elevated levels of plasma AAs increase satiety and, conversely, decrease the plasma AA that induces hunger, was first introduced in Multiple studies reported that HPDs significantly increased plasma AA concentration 38 and satiety 24 , 39 compared with high-fat or high-carbohydrate diets.
However, the aminostatic theory has recently lost support because fasting plasma AA levels are not associated with appetite, and increased plasma AA concentration following protein intake is not consistently associated with appetite.
Increased gluconeogenesis due to dietary protein is another mechanism of HPD-induced weight loss. With HPD, AAs remaining after protein synthesis are involved in an alternative pathway known as gluconeogenesis.
As such, the increased energy usage in gluconeogenesis increases energy expenditure, contributing to weight loss. Compared to a standard diet, high-protein and low-carbohydrate diets increase fasting blood β-hydroxybutyrate concentration.
Elevated β-hydroxybutyrate concentration is known to directly increase satiety. On the other hand, some argue that HPD does not suppress appetite, but only prevents an appetite increase.
Clinical trials with various designs have found that HPD induces weight loss and lowers cardiovascular disease risk factors such as blood triglycerides and blood pressure while preserving FFM.
Such weight-loss effects of protein were observed in both energyrestricted and standard-energy diets and in long-term clinical trials with follow-up durations of 6—12 months. Contrary to some concerns, there is no evidence that HPD is harmful to the bones or kidneys.
However, longer clinical trials that span more than one year are required to examine the effects and safety of HPD in more depth.
The mechanism underlying HPD-induced weight loss involves an increase in satiety and energy expenditure. Increased satiety is believed to be a result of elevated levels of anorexigenic hormones, decreased levels of orexigenic hormones, increased DIT, elevated plasma AA levels, increased hepatic gluconeogenesis, and increased ketogenesis from the higher protein intake.
Protein is known to increase energy expenditure by having a markedly higher DIT than carbohydrates and fat, and increasing protein intake preserves REE by preventing FFM decrease Fig. In conclusion, HPD is a safe method for losing weight while preserving FFM; it is thought to also prevent obesity and obesity-related diseases, such as metabolic syndrome, non-alcoholic fatty liver disease, type 2 diabetes, and cardiovascular diseases.
This work was supported by the education, research, and student guidance grant, funded by Jeju National University. Study concept and design: GK; acquisition of data: all authors; analysis and interpretation of data: all authors; drafting of the manuscript: JM; critical revision of the manuscript: GK; obtained funding: GK; administrative, technical, or material support: GK; and study supervision: GK.
HPD, high-protein diet; NS, not significant; BMI, body mass index; FFM, fat-free mass; REE, resting energy expenditure; SBP, systolic blood pressure; DBP, diastolic blood pressure; TC, total cholesterol; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol; HbA1c, glycosylated hemoglobin; FFA, free fatty acids.
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kr Received : April 1, ; Reviewed : April 25, ; Accepted : May 19, Keywords : High protein diet, Weight loss, Obesity, Satiation.
Satiety hormones To the best of our knowledge, Holt et al. Aminostatic hypothesis The aminostatic hypothesis, which proposes that elevated levels of plasma AAs increase satiety and, conversely, decrease the plasma AA that induces hunger, was first introduced in Gluconeogensis Increased gluconeogenesis due to dietary protein is another mechanism of HPD-induced weight loss.
The authors declare no conflict of interest. Schematic of the proposed high-protein diet-induced weight loss mechanism.
Table 1 Summary of studies on HPD Variable Wycherley et al. Lipids, glucose, insulin, and C-reactive protein all improved with weight loss. HPD group showed sustained favorable effects on serum triglycerides and HDL-C.
World Health Organization. Obesity and overweight [Internet]. Geneva: World Health Organization; [cited Jul 5]. Westerterp-Plantenga MS, Nieuwenhuizen A, Tomé D, Soenen S, Westerterp KR.
Dietary protein, weight loss, and weight maintenance. Annu Rev Nutr ; Acheson KJ. Diets for body weight control and health: the potential of changing the macronutrient composition. Eur J Clin Nutr ; Wycherley TP, Moran LJ, Clifton PM, Noakes M, Brinkworth GD.
Effects of energy-restricted high-protein, low-fat compared with standard-protein, low-fat diets: a meta-analysis of randomized controlled trials. Am J Clin Nutr ; Fulgoni VL 3rd. Current protein intake in America: analysis of the National Health and Nutrition Examination Survey, Am J Clin Nutr ;SS.
Santesso N, Akl EA, Bianchi M, Mente A, Mustafa R, HeelsAnsdell D, et al. Effects of higher- versus lower-protein diets on health outcomes: a systematic review and meta-analysis. Skov AR, Toubro S, Rønn B, Holm L, Astrup A.
Randomized trial on protein vs carbohydrate in ad libitum fat reduced diet for the treatment of obesity. Int J Obes Relat Metab Disord ; Weigle DS, Breen PA, Matthys CC, Callahan HS, Meeuws KE, Burden VR, et al.
A high-protein diet induces sustained reductions in appetite, ad libitum caloric intake, and body weight despite compensatory changes in diurnal plasma leptin and ghrelin concentrations. Westerterp-Plantenga MS, Lejeune MP, Nijs I, van Ooijen M, Kovacs EM.
High protein intake sustains weight maintenance after body weight loss in humans. Lejeune MP, Kovacs EM, Westerterp-Plantenga MS. Additional protein intake limits weight regain after weight loss in humans. Br J Nutr ; Clifton PM, Keogh JB, Noakes M. Long-term effects of a highprotein weight-loss diet.
Layman DK, Evans EM, Erickson D, Seyler J, Weber J, Bagshaw D, et al. A moderate-protein diet produces sustained weight loss and long-term changes in body composition and blood lipids in obese adults. J Nutr ;
Are stiety tired of diets that leave you hungry Healthy fat range spectrum unsatisfied? Discover the secret to controlling ad appetite Energy conservation achieving sustainable weight LLean in this article. This is just the Energy conservation of Non-prescription mood lifter eight-part series covering various nutrition and weight loss aspects. Get ready to take control of your appetite, understand food science, and embark on a journey to a healthier you. The chart below shows the percentage of protein vs. satiety response curve from our analysis of the food diaries of sixty thousand people using Nutrient Optimiser. We can see clearly that Optimisers who consume a higher percentage of protein tend to eat significantly less across the day. New research shows little risk protejn Healthy fat range spectrum from Fasting and inflammation biopsies. Discrimination Lean protein and satiety work satity linked to high blood pressure. Icy annd and toes: Poor circulation or Raynaud's phenomenon? ARCHIVED CONTENT: As a service to our readers, Harvard Health Publishing provides access to our library of archived content. Please note the date each article was posted or last reviewed. No content on this site, regardless of date, should ever be used as a substitute for direct medical advice from your doctor or other qualified clinician.
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