It Takes Guts

It Takes “Guts” to Stop Eat­ing:

Eating Naturally - - Contents - BY WILLIAM B. MILLER, JR., MD

New obe­sity re­search shows overeat­ing may be the fault of mi­crobes in the gut.

If the lengthy na­tional conversation about our obe­sity epi­demic doesn’t take weight off your shoul­ders, you’re not alone. The truth is, our country’s myr­iad di­ets and ar­ti­cles on pinch­ing pounds aren’t clear­ing any weight off our bel­lies, hips, or any­where else.

Those look­ing to lose weight with th­ese pro­grams keep re­vert­ing to their base­line be­cause of bac­te­ria in the gut that can gov­ern our crav­ings.

De­spite th­ese con­cerns, there has been very lit­tle data about the ex­act mech­a­nisms that sep­a­rate those who eat un­til feel­ing full and main­tain a healthy weight and those who con­sume much more food and have a con­se­quent weight prob­lem. Fre­quently, we sim­ply say that one per­son has a more ‘ac­tive’ me­tab­o­lism than the other.

How­ever, new re­search re­veals an ex­ten­sive meta­bolic in­ter­play that has been pre­vi­ously ob­scured. It seems that we have ubiq­ui­tous com­pan­ions un­der­min­ing our self-con­trol and send­ing us un­wanted sig­nals. And I don’t mean friends or rel­a­tives. I’m talk­ing about the tril­lions of mi­crobes that live inside the gut and per­form essen­tial bod­ily func­tions. Pre­vi­ous re­search re­ports have re­vealed that the gut mi­cro­biome has a star­tling range of in­flu­ences. Th­ese micro­organ­isms serve a cru­cial role in me­di­at­ing our im­mune sys­tems, me­tab­o­lism, and cen­tral ner­vous sys­tem, as­sist­ing in nor­mal growth and de­vel­op­ment, and pro­tect­ing us against un­wanted pathogens. Our gut mi­crobes even af­fect our men­tal state and have been linked to de­pres­sion and anx­i­ety.

In ad­di­tion, re­cent re­search has un­cov­ered that gut bac­te­ria play a crit­i­cal role in obe­sity. It is now un­der­stood that cer­tain strains of bac­te­ria are as­so­ci­ated with an in­crease in the con­se­quences of obe­sity such as in­sulin re­sis­tance, type 2 di­a­betes, hy­per­ten­sion, and el­e­vated blood lipids. Un­til now, our work­ing model for ap­petite and sati­ety was based upon the as­sump­tion that this as­pect of obe­sity was de­pen­dent upon an in­trin­sic gut-brain axis of cir­cu­lat­ing gut-tis­sue mol­e­cules and hor­mones and was un­re­lated to the mi­cro­biome.

Our as­sump­tion was when peo­ple eat and be­gin to digest, gut tis­sues send sig­nals of full­ness and sat­is­fac­tion to spe­cific cen­ters in the brain such as the hy­po­thal­a­mus or amyg­dala, in which the nu­tri­tional and sen­sory as­pects of food trig­ger an eat­ing con­trol reg­u­la­tory cir­cuit. How­ever, re­cent re­search has just demon­strated that our gut mi­crobes are di­rectly par­tic­i­pat­ing in that cir­cuit by giv­ing off bioac­tive mol­e­cules that tell us whether we are full or still hun­gry, and sur­pris­ingly, this cir­cuit is de­pen­dent on their as­sess­ment of their own needs. The other cir­cuits cer­tainly ex­ist, but gut bac­te­ria can pro­duce some

Re­cent re­search has un­cov­ered that gut bac­te­ria play a crit­i­cal role in obe­sity. It is now un­der­stood that cer­tain strains of bac­te­ria are as­so­ci­ated with an in­crease in the con­se­quences of obe­sity such as in­sulin re­sis­tance, type 2 di­a­betes, hy­per­ten­sion, and el­e­vated blood lipids. of the same types of chem­i­cals that reg­u­late sati­ety, such as pro­teins and pep­tide hor­mones that are part of the reg­u­la­tory sys­tem of our own cells. So our gut bac­te­ria di­rectly par­tic­i­pate in the body’s trig­ger­ing mech­a­nisms de­ter­min­ing both hunger and full­ness.

There is an im­mense amount of mi­cro­bial life in the stom­ach and in­tes­tine. A new study from re­searchers in France in­ves­ti­gated pro­teins that are pro­duced by one type of bac­te­ria in the stom­ach, known as E. coli. When we eat, th­ese bac­te­ria go through a bipha­sic pat­tern of re­sponse to the nu­tri­ents en­ter­ing our stom­ach. At first, they be­gin to mul­ti­ply very rapidly, pro­duc­ing one set of pro­teins. Af­ter about 20 min­utes of eat­ing, the bac­te­ria stop their rapid growth phase and be­gin to pro­duce other pro­teins that are dis­tinct from the ear­lier prod­ucts of bac­te­rial me­tab­o­lism pro­duced dur­ing the most ac­tive pe­riod of their re­pro­duc­tive cy­cle. It is the sec­ond type of protein that seems to di­rectly in­flu­ence our feel­ings of sati­ety.

To prove the con­nec­tion, the re­searchers in­jected this sec­ond type of protein into ro­dents that had not been fed or were only given small amounts of food. Upon ad­min­is­tra­tion of this spe­cific bac­te­rial protein, the un­fed ro­dents ei­ther sig­nif­i­cantly di­min­ished their food in­take or stopped eat­ing com­pletely. This ex­per­i­ment demon­strated that the bac­te­rial pro­teins from E. coli are in­volved in the same path­ways of hor­monal stim­u­la­tion used by our own cells to is­sue sig­nals to the brain in­di­cat­ing sen­sa­tions of hunger and full­ness. Based on this re­search, it is es­ti­mated that it takes an in­crease of about 1 bil­lion ex­tra bac­te­ria in the stom­ach be­fore the growth phase switches from ac­tive growth to the more static phase as­so­ci­ated with the pro­duc­tion of pro­teins linked to sati­ety.

Ad­di­tional re­search should clar­ify fur­ther as­pects of this dy­namic and hope­fully lead to bet­ter treat­ments for obe­sity in the fu­ture. It is be­com­ing clear that any path­way to­ward real suc­cess will be based upon a deeper un­der­stand­ing of how the mi­cro­biome in­ter­acts with our in­trin­sic reg­u­la­tory mech­a­nisms. As for my own gut mi­crobes, I’m pretty cer­tain that they pre­fer cho­co­late chip cook­ies. For now, that’s go­ing to be my ex­cuse.

William B. Miller, Jr., MD has been a physi­cian in aca­demic and pri­vate prac­tice for more than 30 years. He is the author of The Mi­cro­cosm Within: Evo­lu­tion and Ex­tinc­tion in the Hologenome. // themi­cro­cosmwithin.com

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