Stop snacking for better metabolic health

Arrêter de grignoter pour une meilleure santé métabolique

Stop snacking: how and why?

Snacking is now a common part of our eating habits. However, in the past, it was not common to eat between meals. What are the impacts on metabolic health? How can we stop snacking between meals?

One theory behind the emergence of snacks is that they were introduced following the marked increase in carbohydrates in our meals. Indeed, when the meal is digested, there is often a significant and rapid increase in post-prandial blood sugar, which is followed by a drop that can be felt as a lack of energy or hunger. Snacks, often also rich in carbohydrates, are therefore there to raise blood sugar levels until the next meal. However, unstable and constantly high blood sugar is really not desirable for metabolic health. 1,2

So let's see what impacts high blood sugar and insulin levels can have and what helps sustain us until the next meal without feeling hungry.


Impacts of high blood sugar:

  • When blood sugar is high, it damages the endothelial cells of blood vessels and the epithelial cells of the intestine, creating inflammation. This is the mechanism that partly explains the appearance of diabetic retinopathies, neuropathies and nephropathies. 2
  • A large influx of glucose or fructose into the mitochondria creates more free radicals that can damage the mitochondria and the cell itself. Again, this oxidative damage will lead to inflammation. 2,3
  • High blood sugar increases glycation, a reaction that causes a glucose molecule to form a covalent bond with a protein, making it nonfunctional and harder to break down for recycling. This contributes to cellular aging and even the appearance of wrinkles when this reaction occurs in the skin's collagen! 2,4,5
  • Sugar metabolism increases the production of uric acid, which inhibits an enzyme in the blood vessels called nitric oxide synthase, which is responsible for producing nitric oxide for the blood vessels. Nitric oxide, among other things, allows vasodilation and therefore the regulation of blood pressure. It is a molecule that plays a vasoprotective and anti-atherosclerosis role. 6
  • Uric acid also blocks an enzyme in the mitochondria (CPT1) that prevents carnitine from transporting fatty acids into the mitochondria to produce ATP, the cellular energy. High uric acid levels are linked to impaired lipid metabolism. 7
  • Fructose acts exactly like alcohol in the liver, promoting the accumulation of fat and thus the development of non-alcoholic fatty liver disease. Fructose also inhibits three enzymes in the mitochondria, making them much less efficient. In other words, it decreases metabolism. 3


Impacts of high insulin:

  • Insulin resistance is linked to the increase in ApoB lipoproteins, caused among other things by various dysfunctions of its regulation in the liver. ApoB is found on LDL and VLDL, which are called bad cholesterol. The higher the ApoB level, the more atheromatous plaques form in the arteries. 8
  • When insulin is present, the body is in storage mode. Insulin stimulates adipocytes, the fat cells, to store more fat. However, contrary to what one might think, it is not the number of fat cells that increases, but rather the amount of fat contained in their vacuoles. When these are too full, the membranes become fragile and damaged, which leads to inflammatory reactions in the cell. 9
  • Insulin in large quantities has the ability to block leptin receptors and cause leptin resistance. Leptin is a satiety hormone secreted by adipocytes to signal that we have enough energy reserves (fatty acids). Since insulin blocks the receptors, even though leptin is present in large quantities, our brain cannot receive its message. This has the effect of making us believe that we are lacking food and our brain will want to do everything to ensure that we conserve our energy, it is a question of survival! So it is not that you lack motivation to move, it is that your brain is trying to keep you alive by limiting your energy expenditure. 10
  • Insulin decreases the excretion of sodium by the kidneys, so the kidneys retain more water as a result, which can influence the increase in blood pressure. 11

What helps keep us going until the next meal without feeling hungry:

As you probably know, including protein and good fats in each of our meals is very important for a healthy and balanced diet. These will help provide a longer-lasting feeling of satiety. Indeed, when the body perceives that it has received enough protein, hormones (PYY and GLP-1) are secreted to reduce appetite and the synthesis of ghrelin (hunger hormone) will also be reduced. 12,13

For those who enjoy a little dessert at the end of the meal, an option like the "snack square" will satisfy your sweet tooth and add more protein and healthy fats to the meal. Post-prandial blood sugar levels will be kept more stable, keeping us full until the next meal.

You'll understand that none of this has anything to do with calorie restriction or encouraging hunger. On the contrary, it's important to eat your fill in order to give your body everything it needs and maintain a healthy metabolism. However, by eating the right foods that support us, we'll find ourselves able to space out our meals without difficulty, which will be greatly beneficial for our metabolic health.

Additionally, avoiding late-night snacks will help you sleep better. Even better, if you can extend the time between dinner and lunch until 2 p.m. or even 4 p.m. (eating between 8 a.m. and 6 p.m. or 10 a.m. and 6 p.m., for example), you can reap the metabolic health and cellular repair benefits of intermittent fasting! 14


References:

1 Pimenta AM, Bes-Rastrollo M, Gea A, Sayón-Orea C, Zazpe I, Lopez-Iracheta R, Martinez-Gonzalez MA. Snacking between main meals is associated with a higher risk of metabolic syndrome in a Mediterranean cohort: the SUN Project (Seguimiento Universidad de Navarra). Public Health Nutr. 2016 Mar;19(4):658-66. doi:10.1017/S1368980015001342. Epub 2015 May 11. PMID: 25958949; PMCID:PMC10270996.

2 Biplab Giri, Sananda Dey, Tanaya Das, Mrinmoy Sarkar, Jhimli Banerjee, Sandeep Kumar Dash, Chronic hyperglycemia mediated physiological alteration and metabolic distortion leads to organ dysfunction, infection, cancer progression and other pathophysiological consequences: An update on glucose toxicity, Biomedicine & Pharmacotherapy, Volume 107, 2018, Pages 306-328, ISSN 0753-3322, https://doi.org/10.1016/j.biopha.2018.07.157.

3 Lustig RH. Fructose: it's "alcohol without the buzz". Adv Nutr. 2013 Mar 1;4(2):226-35. doi:10.3945/an.112.002998. PMID: 23493539;PMCID: PMC3649103.

4 Kim CS, Park S, Kim J. The role of glycation in the pathogenesis of aging and its prevention through herbal products and physical exercise. J Exercise Nutrition Biochem. 2017 Sep 30;21(3):55-61. doi: 10.20463/jenb.2017.0027. PMID: 29036767; PMCID: PMC5643203.

5 Zheng W, Li H, Go Y, Chan XHF, Huang Q, Wu J. Research Advances on the Damage Mechanism of Skin Glycation and Related Inhibitors. Nutrients. 2022 Nov 1;14(21):4588. doi:10.3390/nu14214588. PMID: 36364850; PMCID: PMC9655929.

6 Förstermann U, Sessa WC. Nitric oxide synthases: regulation and function. Eur Heart J. 2012 Apr;33(7):829-37, 837a-837d. doi: 10.1093/eurheartj/ehr304. Epub 2011 Sep 1. PMID: 21890489; PMCID: PMC3345541.

7 Ma L, Wang J, Ma L, Ge Y, Wang XM. The effect of lipid metabolism disorder on patients with hyperuricemia using Multi-Omics analysis. SciRep. 2023 Oct 24;13(1):18211. doi:10.1038/s41598-023-45564-8. PMID: 37875599; PMCID: PMC10598229.

8 Haas ME, Attie AD, Biddinger SB. The regulation of ApoB metabolism by insulin. Trends Endocrinol Metab. 2013 Aug;24(8):391-7. doi: 10.1016/j.tem.2013.04.001. Epub 2013 May 27. PMID: 23721961; PMCID: PMC3810413.

9 Bulbul Ahmed, Rifat Sultana, Michael W. Greene, Adipose tissue and insulin resistance in obese, Biomedicine & Pharmacotherapy, Volume 137, 2021, 111315, ISSN 0753-3322, https://doi.org/10.1016/j.biopha.2021.111315.

10 Sam Dagogo-Jack, Leptin and Insulin Sensitivity: Endogenous Signals of Metabolic Homeostasis, The Journal of Clinical Endocrinology & Metabolism, Volume 109, Issue 5, May 2024, Pages e1402–e1403, https://doi.org/10.1210/clinem/dgad653

11 DeFronzo RA. The effect of insulin on renal sodium metabolism. A review with clinical implications. Diabetology. 1981 Sep;21(3):165-71. doi:10.1007/BF00252649. PMID: 7028550.

12 Belza A, Ritz C, Sørensen MQ, Holst JJ, Rehfeld JF, Astrup A. Contribution of gastroenteropancreatic appetite hormones to protein-induced satiety. Am J Clin Nutr. 2013 May;97(5):980-9. doi:10.3945/ajcn.112.047563. Epub 2013 Mar 6. PMID: 23466396.

13 Ali Kohanmoo, Shiva Faghih, Masoumeh Akhlaghi, Effect of short- and long-term protein consumption on appetite and appetite-regulating gastrointestinal hormones, a systematic review and meta-analysis of randomized controlled trials, Physiology & Behavior, Volume 226, 2020, 113123, ISSN 0031-9384, https://doi.org/10.1016/j.physbeh.2020.113123.

14 Vassek, J. “Autophagy Fasting: What You Need to Know Before Starting,” LifeMD. October 9, 2023 (accessed January 30, 2025) https://lifemd.com/learn/autophagy-fasting#:~:text=Short%2Dterm%20activation%3A%20Shorter%20fasting,and%20contribute%20to%20overall%20health.

Maison Jacynthe disclaims all liability. All information contained in this article is not intended to replace justified allopathic treatment or disregard the expertise of the medical profession. It is up to each individual to take charge of their own health, to inform themselves, and to make the necessary changes to improve their condition. Therapeutic supervision by a qualified healthcare professional is strongly recommended.

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