Yu gɛt ay blɔd shuga bak na mɔnin? Dis kin bi bikɔs ɔf di ‘Dawn Phenomenon’!

If yu gɛt dayabitis, yu dɔn ɛva notis se yu blɔd shuga kin go ɔp wantɛm wantɛm we yu wek na mɔnin? Yu go de wɔnda wetin mek dis kin apin pan ɔl we yu de tek yu mɛrɛsin na nɛt ɛn kɔntrol di tin dɛn we yu de it. Nɔ wɔri, wan rizin fɔ dis kin bi di ‘Dawn Phenomenon’ we wi de tɔk bɔt tide. Lɛ wi si wetin i bi, wetin mek i kin apin, ɛn aw fɔ avɔyd am.

Wetin na di Dawn Phenomenon, dis inkris na di blɔd shuga na di ali mɔnin?

Fɔ tɔk am simpul wan, di ‘Dawn Phenomenon’ na natura l inkris na di blɔd shuga lɛvɛl na di ali mɔnin bikɔs ɔf sɔm ɔmon dɛm we wi bɔdi de mek. Dis kin jɔs afɛkt pipul dɛn we gɛt dayabitis. Dis na di men rizin wae mek yu wae gɛt shuga kin gɛt bɔrku shuga na yu blɔd (haypa glycemia) na mɔnin.

Bɔt mɛmba se nɔto dis nɔmɔ de mek di blɔd shuga go ɔp na mɔnin. Bɔku ɔda rizin dɛn kin de:

• Nɔto inof mɛrɛsin: Sɔntɛnde, di amount of mɛrɛsin we dɛn de tek na nɛt nɔ kin inof bay mɔnin, ɛn di ifɛkt we i gɛt kin lɔs.
• Mismatching medication and food: Nɔ de kɔl di kɔrɛkt amount ɛn tɛm fɔ tek mɛrɛsin wit dina.
• Somogyi effect: Dis na di opozit smɔl. Sɔntɛnde, di insulin we dɛn kin pul na nɛt kin bɔku, ɛn dis kin mek di blɔd shuga go dɔŋ bad bad wan wantɛm wantɛm. Dɔn di bɔdi kin pul wan ɔmon fɔ ansa dis, ɛn dis kin mek di blɔd shuga go ɔp bak. Dɛn kɔl dis ‘Somogyi ifɛkt’.

Aw kɔmɔn tin dis?

Dawn Phenomenon na rili wan sik wae kin pasmak pan pipul dɛm wae gɛt shuga. Risach dɔn sho se i kin afɛkt pas 50% pan pipul dɛm wae gɛt Tayp 1 ɔ Tayp 2 dayabitis . Dis min se nɔto yu wan de.

Wetin na di sayn dɛm fɔ dis?

Di men sayn fɔ di ‘Dawn Phenomenon’ na we di blɔd shuga lɛvɛl de go ɔp na di mɔnin. Yu kin si dis we yu wek na mɔnin ɛn chɛk yu glukomita, ɔ if yu yuz CGM (Continuous Glucose Monitoring) divays. Bɔku tɛm, di ‘Dawn Phenomenon’ kin mek wan patɛn we de mek di blɔd shuga go ɔp na mɔnin fɔ sɔm dez insay wan row.

Dipen pan aw yu blɔd shuga ay, yu kin gɛt sɔm kayn sik dɛn lɛk dis we yu wek na mɔnin:

• Fɔ fil se yu tɔsti pasmak (polydipsia).
• Fɔ fil mɔ angri.
• Fɔ pis bɔku tɛm.
• Ed de at.
• Fɔ vɛks, fɔ vɛks.
• Di vishɔn we nɔ klia.

Imajin, pɔsin de we nem Malani, we gɛt dayabitis. I kin chɛk in blɔd shuga ɛvri mɔnin. Fɔ tri ɔ 4 dez insay wan row, in blɔd shuga na mɔnin pas 200mg/dL. I kin kɔntrol bak di it we i de it na nɛt ɛn i kin tek in mɛrɛsin di rayt tɛm. I kin fil bad bad wan. I kin fil taya smɔl we i wek na mɔnin, ɛn i kin tɔsti bad bad wan. Sɔntin lɛk dis dɔn apin to yu? Dɔn i pɔsibul se na di ‘Dawn Phenomenon’.

Wetin mek dis de apin?

Dis na smɔl sayɛns tru tin, bɔt a go tɔk am simpul wan. na di ali mכnin – dat na bitwin 3 εn 8 na di mכnin – wi bכdi de rilis wan siriכs כmon dεm. Di men wan dɛn na kɔtisol ɛn di ɔmon we de mek pɔsin gro . Dɛn ɔmon dɛn ya kin mek wi liva mek mɔ glukɔs , we na shuga. Dis glukose de ɛp fɔ wek wi na mɔnin ɛn gi wi di ɛnaji fɔ bigin di de. We dɛn mek mɔ glukɔs, di shuga we de na wi blɔd kin go ɔp.

Naw, if yu nɔ gɛt dayabitis, yu pankrias de ansa dis ɛn i de mek inof insulin fɔ kɔntrol yu blɔd shuga. Bɔt if yu gɛt dayabitis, yu pankrias ɔ nɔ de mek ɛni insulin atɔl, ɔ di mɔnt we i de mek nɔ go du fɔ kɔntrol di ay blɔd shuga. Sɔntɛnde , insulin resistance , we min se yu bɔdi in sɛl dɛn nɔ de ansa fayn to insulin, kin bi bak wan kɔz.

Fɔ tɔk di kɔrɛkt tin, we di bɔdi de rɛdi fɔ wek na mɔnin, dis natura ‘alarm system’ na di bɔdi de mek di blɔd shuga go ɔp. Pan ɔl we dɛn kin kɔntrol dis na pɔsin we nɔ gɛt shuga in bɔdi, pɔsin we gɛt shuga in bɔdi nɔ kin ebul fɔ du am fayn.

Aw yu no dis klia wan?

di bεst we fכ no kכrekt if di ‘Dawn Phenomenon’ na di kכz fכ hכy bכdi shuga na mכnin na fכ yuz CGM (Continuous Glucose Monitoring) .

CGM na divays we yu kin wɛr fɔ wach yu blɔd glukɔs lɛvɛl 24 awa ɛvride. Fɔ tɔk di kɔrɛkt tin, dis CGM divays de mɛzhɔ yu blɔd shuga lɛvɛl ɛvri sɔm minit ɛn yuz da data de fɔ mek wan grafik. Dis kin gi yu wan kɔmplit pikchɔ bɔt aw yu blɔd shuga lɛvɛl de chenj as tɛm de go.

Di bɛnifit fɔ yuz CGM, pas fɔ tek blɔd na yu finga bifo yu go slip ɛn afta yu wek na mɔnin ɛn chɛk yu blɔd shuga wit glukomita, na dat yu kin no klia wan if yu blɔd shuga dɔn drɔp wantɛm wantɛm (haypoglycemia) na nɛt. If na so, i min se yu nɔ de ɛkspiriɛns di ‘Dawn Phenomenon’, bɔt di ‘Somogyi effect’ we wi bin dɔn tɔk bɔt.

Ivin if yu nɔ yuz CGM, dɔktɔ dɛn kin luk di we aw yu blɔd shuga de rid fɔ sɔm dez ɛn dɛn kin sɔprayz se di ‘Dawn Phenomenon.’ Na dat mek i rili impɔtant fɔ kip yu blɔd shuga ridin.

Wetin na di tritmɛnt fɔ dis?

Di bɛst tritmɛnt fɔ di ‘Dawn Phenomenon’ na fɔ yuz insulin pɔmp fɔ gi insulin. Di mɛrɛsin dɛn we dɛn kin tek fɔ mɛn sik dɛn we dɛn kin it, nɔ kin ɛp bɔku wit di ‘Dawn Phenomenon’. Dɔn bak, insulin injɛkshɔn we de wok fɔ lɔng tɛm nɔ go gɛt bɔku ɛfɛkt pan dis.

Yu dɔktɔ kin ajɔst yu basal insulin rit ɛn mek yu insulin pɔmp gi yu smɔl mɔ insulin ɔtomɛtik wan na mɔnin. Dis kin ɛp fɔ mek yu blɔd shuga nɔ go ɔp na mɔnin.

Bɔt if yu nɔ de yuz insulin pɔmp, ɔ if yu nɔ de tek insulin atɔl, yu ɛn yu dɔktɔ go nid fɔ du sɔm tray ɛn mistek fɔ fɛn di bɛst mɛrɛsin ɛn chenj dɛn layf fɔ kɔntrol di mɔnin blɔd shuga we de go ɔp bikɔs ɔf di ‘dawn phenomenon’. Fɔ ɛgzampul, yu dɔktɔ go advays yu fɔ mek yu ɛksesaiz mɔ na ivintɛm ɛn fɔ mek yu gɛt mɔ prɔtin na yu dina we yu kɔmpia am to di kabɔhaydrɛt.

Yu nɔ tink se dɛn go ebul fɔ stɔp dis?

Bikɔs di ‘Dawn Phenomenon’ na rizɔlt fɔ wan natura prɔses we de apin na di bɔdi, natin nɔ de we yu go rili du fɔ mek i nɔ apin kpatakpata.

Bɔt if yu yuz insulin pɔmp, yu kin ajɔst yu basal insulin rit akɔdin to yu dɔktɔ in instrɔkshɔn ɛn kɔntrol di fiuja mɔnin blɔd shuga spayk bikɔs ɔf di ‘dawn phenomenon’ to sɔm mak.

Wetin na di sayd ɛfɛkt dɛm we dis kin gɛt?

Di men sayd ifekt we yu nɔ trit mɔnin ay blɔd shuga bikɔs ɔf di ‘dawn phenomenon’ na we yu A1C de go ɔp. Wan A1C tɛst de sho yu avɛrej blɔd glukɔs (shuga) lɛvɛl fɔ di pas tri mɔnt.

Di mɔ yu A1C lɛvɛl go ɔp, na di mɔ yu go gɛt prɔblɛm dɛn we gɛt fɔ du wit dayabitis. Dis risk kin hεvi spεshal if yu A1C lεvεl de hכy fכ plεnti ia. Di prɔblɛm dɛn we kin apin to pɔsin we gɛt dayabitis kin bi:

• Di prɔblɛm dɛn we kin apin to pɔsin in yay (Retinopathy) .
• Prɔblɛm dɛn na di kidni (Nephropathy) .
• Nyuropati we pɔsin kin gɛt
• At sik

Risach dɔn sho se if pipul dɛm wae gɛt shuga kin kip dɛn A1C lɛvɛl ɔltɛm ɔnda 7% , dɛn kin ridyus dɛn risk fɔ gɛt prɔblɛm dɛm wae gɛt fɔ du wit dayabitis.

Di ‘Dawn Phenomenon’ kin bi prɔblɛm we de kɔntinyu, we min se if dɛn nɔ trit am, di blɔd shuga lɛvɛl kin de ɔp fɔ sɔm awa ɛvride. Dis kin mek yu gɛt mɔ prɔblɛm wit dayabitis as tɛm de go.

Ustɛm a fɔ go to dɔktɔ?

If yu kin gɛt ay shuga na yu blɔd ɔltɛm na mɔnin, i impɔtant fɔ tɔk to yu dɔktɔ we de ɛp yu fɔ kɔntrol yu dayabitis. I kin chɛk yu blɔd shuga lɛvɛl, no if dis na bikɔs ɔf di Dawn Phenomenon, ɛn i kin tɛl yu di rayt tritmɛnt fɔ yu.

Fɔ ɛkspiriɛns di ‘dawn phenomenon’, we na di blɔd shuga lɛvɛl we de go ɔp na mɔnin, kin rili mek yu at pwɛl ɛn mek yu at pwɛl. Bɔt mɛmba se nɔto yu fɔlt. No wan-sayz-fit-ɔl we nɔ de fɔ manej yu mɔnin shuga spayk. So i kin tek sɔm tɛm fɔ fɛn di rayt tritmɛnt fɔ yu. Yu dɔktɔ kin ɛp yu fɔ kam wit di bɛst plan. So nɔ shem fɔ aks fɔ ɛp. If yu tek akshɔn naw, dat go ɛp yu fɔ avɔyd di bad tin dɛn we go apin to yu fɔ lɔng tɛm.

Di tin we impɔtant pas ɔl we yu fɔ mɛmba

Okay, so a op se yu don andastan beta nau fo di ‘Dawn Phenomenon’ we wi tok abaut. Mɛmba se if yu de liv wit dayabitis, no se di shuga na yu blɔd de go ɔp na mɔnin.

Dis nɔto yu fɔlt, ɛn sɔlv dɛn de fɔ dis.

• Tɔk to yu dɔktɔ bɔt dis opin wan.
• Kip kɔrɛkt rɛkɔd fɔ yu blɔd shuga, it, ɛn mɛrɛsin.
• If yu kin yuz CGM, di data we i de gi yu rili valyu.
• Tɔk to yu dɔktɔ bɔt insulin pɔmp, i kin bi gud sɔlv fɔ dis.
• Nɔr panik ɔr pwɛl hat, woke wit yu dɔktɔ fɔ fɛn di bɛst sɔlv fɔ yu.

Mɛmba se yu kin liv fayn ɛn gladi layf wit dayabitis. I jɔs nid fɔ no, kia, ɛn fala yu dɔktɔ in advays. Una gɛt fayn fayn de!

` Dawn Phenomenon, dayabitis, mɔnin blɔd shuga inkris, haypa glycemia, Somogyi ifɛkt, insulin pɔmp, A1C