Weight Gain and Gut Health: The Surprising Link
by Chris D. Meletis, ND
There are many factors that can affect how easily people gain or lose weight. These include everything from balanced blood sugar to lack of exercise to sleep loss to toxins in the environment (as discussed in the January newsletter). But one of the more surprising reasons why weight management programs can be unsuccessful is the failure to recognize the connection between gut health and body weight. In fact, when the other factors listed above aren’t tended to, the inflammation that occurs in the gut and in the body as a result may be a primary reason for weight gain.
Weight management is a major concern for many individuals as reflected by the fact that the number of people with larger than normal body mass index has increased 60 percent within the past 20 years. According to the Centers for Disease Control, 33 percent of adult Americans have a larger than normal body mass index and 66 percent of American adults are overweight.1-2 Deaths related to having a larger than normal body mass index have climbed to more than 300,000 a year—second only to tobacco-related deaths.1-2
To bring these statistics home on a more personal level, struggling with weight loss can be a highly frustrating endeavor. Looking into all the potential reasons behind why a person has gained weight can help get to the root cause of the issue and result in a successful weight management program. Consequently, this article will address an often-overlooked reason behind weight gain—an imbalanced inflammatory response in the gut.
Research spanning the past two decades has revealed that being overweight is a pro-inflammatory condition. It is, in fact, a vicious circle since an imbalanced inflammatory response can trigger weight gain and being overweight itself increases the inflammatory response.
The Forgotten Organ
The gut microbiota—in other words the friendly flora in the intestines—play a role in helping the intestines achieve a balanced inflammatory state. In fact, intestinal flora perform actions that are similar to those of an organ, leading researchers to suggest that the gut flora is a “forgotten organ.”3
At birth, the human gut is devoid of the vitally important flora. It’s then colonized with bacteria from the mother and the environment. During childhood, the complexity of the gut flora is increased and ultimately, adult human intestinal tracts contain 150-fold more bacterial genes than human genes.4
Studies have shown that the intestinal flora play an important role in both balancing inflammation and controlling body weight. Intestinal flora influence nutrient acquisition and energy balance and consequently have a big part to play in helping control body weight. The make up of intestinal flora can change during poor eating habits or antibiotic intake. These changes help contribute to increased intestinal permeability and lead to the development of a low-grade inflammatory state that contributes to weight gain.5
Research is beginning to reveal that the types of flora in the intestines determine whether a person is lean or overweight. In animal studies, it was shown that the majority of the intestinal flora consists of two phyla, the Bacteroidetes and the Firmicutes, and that the amount of these two phyla differs among lean and obese mice. Obese mice had a higher proportion of Firmicutes to Bacteroidetes (50\% greater) than the lean mice. The same results were found in humans with a higher than normal body mass index compared to lean subjects. Researchers believe the explanation for this is because the presence of Firmicutes results in a more complete metabolism of a given energy source than do Bacteroidetes, encouraging more efficient calorie absorption and subsequent weight gain.6
When researchers colonized lean mice with the intestinal flora from obese mice, it led to increased total body fat in the lean mice despite a lack of change in diet.6
In addition, gut microbes also influence the metabolism of cells in tissues outside of the intestines—in the liver and fat tissue for example—and therefore help maintain lipid and glucose balance, as well as balance inflammatory responses, throughout the body.7
The Leptin-CRP Link
One important marker of inflammatory responses in the body is C-reactive protein (CRP). Studies have found that CRP has an interesting effect on the appetite-regulating hormone known as leptin. Elevated CRP may trigger leptin resistance by inhibiting the binding of leptin to its receptors.8 When the body develops leptin resistance, it becomes immune to the appetite-regulating effects of this hormone.
In studies of leptin-resistant animals fed high-fat meals, prebiotics, which serve as nourishment for the healthy intestinal flora, reduced the imbalanced inflammatory responses seen in the animals as well as improved leptin sensitivity.9
Healthy Gut = Healthy Weight
Imbalanced inflammatory responses in the intestines can weaken the gut epithelium, the layer of cells lining the intestinal walls. The gut epithelium is a barrier between the “outside” and “inside” world. The epithelium absorbs nutrients, ions and water while at the same time protecting the “inside” world from potentially harmful toxins, irritants and undesirable organisms that also exist in the gut lumen. The health of an individual depends upon the efficient digestion and absorption of all required nutrients from the diet.10
However, breakdown of the epithelium is associated with gut inflammation. If the gut epithelium becomes permeable, nutrients escape rather than being absorbed. Several recent studies have provided compelling new evidence to suggest that changes in epithelial barrier function and an imbalanced inflammatory response are associated with and may even lead to altered regulation of body weight and glucose metabolism. Recent evidence supports the hypothesis that alteration of gut epithelial function, associated with changes in the gut flora, will disturb the pathways controlling food intake and body weight.10
Prebiotics improve this imbalanced inflammatory response, strengthen the intestinal barrier and enhance the integrity of tight-junctions, the spaces between cells that line the intestines.11 Tight junctions are normally sealed. However, when the intestinal lining becomes irritated, the junctions loosen and allow unwanted larger molecules in the intestines to pass through into the blood.
In addition to taking a good probiotics/prebiotic supplement, an excellent way to strengthen the gut barrier is to consume the combination of natural substances found in GI Cell Support: L-glutamine, deglycyrrhizinated licorice (DGL), N-acetyl glucosamine, marshmallow (Althaea officinalis) root, berberine sulfate, cabbage leaf, slippery elm (Ulmus rubra), phosphatidylcholine and gamma oryzanol. These substances help strengthen the colon lining, soothe and protect mucous membranes and support healthy inflammatory responses in the GI Tract.12-22
Other Anti-Inflammatory Strategies
There are other effective ways to balance inflammatory responses in the colon and throughout the body. One of those ways is to consume a low-glycemic-index diet,23 ideally one that includes optimal amounts of fiber. Eating a low-glycemic diet involves eating foods that have a minimal effect on blood sugar. Researchers conducted a randomized, crossover feeding study testing low- compared to high-glycemic diets on biomarkers of inflammation and markers associated with being overweight in healthy adults. Eighty participants were given a low-glycemic diet for 28 days then switched to a high-glycemic diet for 28 days. Blood was drawn from fasting participants at the beginning and end of each feeding period and serum concentrations of high-sensitivity CRP, serum amyloid A, IL-6, leptin, and adiponectin were measured. Among participants with high-body fat mass (greater than 32 percent for males and greater than 25 percent for females), the low-glycemic diet reduced CRP, indicating it had a balancing effect on inflammatory responses.24
Moderate exercise is also important to maintain a healthy inflammatory response as is restorative sleep. Depriving oneself of sufficient sleep results in elevated inflammatory mediators as well as insulin inefficiency, which plays a contributory role in increased inflammation.25
Taking steps to reduce stress is also important. There is a well-known connection between stress and imbalanced inflammatory responses in the intestinal tract.
Researchers have found that lifestyle changes can be highly effective in balancing inflammatory responses.26
Conclusion
Less than optimal gut health is an overlooked reason why weight management programs can fail. Creating balanced inflammatory responses in the intestinal tract by 1) eating a low-glycemic diet 2) getting sufficient sleep 3) exercising 4) reducing stress and 5) taking probiotics/prebiotics and GI Cell Support can go a long way in supporting healthy weight goals.
References
1. Centers for Disease Control and Prevention website, http://www.cdc.gov/obesity/index.html accessed January 5, 2012.
2. Bharat B. Aggarwal Annu Rev Nutr. Targeting Inflammation-Induced Obesity and Metabolic Diseases by Curcumin and Other Nutraceuticals. 2010 August 21;30:173-199.
3. O’Hara AM, Shanahan F. The gut flora as a forgotten organ. EMBO Rep. 2006 Jul;7(7):688-93.
4. Bäckhed F. Programming of host metabolism by the gut microbiota. Ann Nutr Metab. 2011;58 Suppl 2:44-52.
5. Frazier TH, DiBaise JK, McClain CJ. Gut microbiota, intestinal permeability, obesity-induced inflammation, and liver injury. JPEN J Parenter Enteral Nutr. 2011 Sep;35(5 Suppl):14S-20S.
6. Kallus SJ, Brandt LJ. The intestinal microbiota and obesity. J Clin Gastroenterol. 2012 Jan;46(1):16-24.
7. Delzenne NM, Neyrinck AM, Bäckhed F, Cani PD. Targeting gut microbiota in obesity: effects of prebiotics and probiotics. Nat Rev Endocrinol. 2011 Aug 9;7(11):639-46.
8. Spruijt-Metz D, Emken BA, Spruijt MR, Richey JM, Berman LJ, Belcher BR, Hsu YW, McClain AD, Lane CJ, Weigensberg MJ. CRP Is Related to Higher Leptin Levels in Minority Peripubertal Females Regardless of Adiposity Levels. Obesity (Silver Spring). 2011 Mar 24. Published Online Ahead of Print.
9. Everard A, Lazarevic V, Derrien M, Girard M, Muccioli GM, Neyrinck AM, Possemiers S, Van Holle A, François P, de Vos WM, Delzenne NM, Schrenzel J, Cani PD. Responses of gut microbiota and glucose and lipid metabolism to prebiotics in genetic obese and diet-induced leptin-resistant mice. Diabetes. 2011 Nov;60(11):2775-86.
10. Raybould H. Gut Microbiota, Epithelial Function and Derangements In Obesity. J Physiol. 2011 Dec 19. Published Online Ahead of Print
11. Cani PD, Possemiers S, Van de Wiele T, Guiot Y, Everard A, Rottier O, Geurts L, Naslain D, Neyrinck A, Lambert DM, Muccioli GG, Delzenne NM. Changes in gut microbiota control inflammation in obese mice through a mechanism involving GLP-2-driven improvement of gut permeability. Gut. 2009 Aug;58(8):1091-103.
12. Miller AL. Therapeutic considerations of L-glutamine: a review of the literature. Altern Med Rev. 1999;4:239-48.
13. van Marle J, Aarsen PN, Lind A, van Weeren-Kramer J. Deglycyrrhizinised liquorice (DGL) and the renewal of rat stomach epithelium. Eur J Pharmacol. 1981;72:219-25.
14. Burton AF, Anderson FH. Decreased incorporation of 14C-glucosamine relative to 3H-N-acetyl glucosamine in the intestinal mucosa of patients with inflammatory bowel disease. Am J Gastroenterol. 1983;78:19-22.
15. Newall CA, Anderson LA, Philpson JD. Herbal Medicine: A Guide for Healthcare Professionals. London, UK: The Pharmaceutical Press, 1996.
16. Martindale W. Martindale the Extra Pharmacopoeia. Pharmaceutical Press, 1999.
17. Fukuda K, Hibiya Y, Mutoh M, et al. Inhibition by berberine of cyclooxygenase-2 transcriptional activity in human colon cancer cells. J Ethnopharmacol. 1999;66:227-33.
18. van Poppel G, Verhoeven DT, Verhagen H, Goldbohm RA. Brassica vegetables and cancer prevention. Epidemiology and mechanisms. Adv Exp Med Biol. 1999;472:159-68.
19. Cheney G (1952). Vitamin U Therapy of Peptic Ulcer. California Medicine. 77(4):248-252.
20. Stremmel W, Ehehalt R, Autschbach F, Karner M. Phosphatidylcholine for steroid-refractory chronic ulcerative colitis: a randomized trial. Ann Intern Med. 2007 Nov 6;147(9):603-10.
21. Cicero AFG, Gaddi A. Rice Bran and Gamma-Oryzanol in the treatment of hyperlipoproteinemias and other conditions. Phytotherapy Research. 15(4):277-289.
22. Seetharamaiah GS, Chandrasekhara N. Effect of oryzanol on cholesterol absorption and biliary and fecal bile acids in rats. Indian J Med Res. 1990;92:471-5.
23. Esfahani A, Wong JM, Mirrahimi A, Srichaikul K, Jenkins DJ, Kendall CW. The glycemic index: physiological significance. J Am Coll Nutr. 2009 Aug;28 Suppl:439S-445S.
24. Neuhouser ML, Schwarz Y, Wang C, Breymeyer K, Coronado G, Wang CY, Noar K, Song X, Lampe JW. A Low-Glycemic Load Diet Reduces Serum C-Reactive Protein and Modestly Increases Adiponectin in Overweight and Obese Adults. J Nutr. 2011 Dec 21. Published Online Ahead of Print
25. [No authors listed] [Sleep and metabolic disorders]. [Article in Serbian] Glas Srp Akad Nauka Med. 2011;(51):5-25.
26. Garanty-Bogacka B, Syrenicz M, Goral J, Krupa B, Syrenicz J, Walczak M, Syrenicz A. Changes in inflammatory biomarkers after successful lifestyle intervention in obese children. Endokrynol Pol. 2011;62(6):499-505.
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