रात्री उशिरा झोपणे भूक आणि खाण्याची इच्छा वाढव ते

 

संदर्भ

पोषक तत्वे. 2023 एप्रिल 23; 15(9): 2035. doi: 10.3390/nu15092035

रात्री उशिरा झोप कमी झाल्यास, पण लवकर झोप कमी न झाल्यास, न्यूरोएंडोक्राइन भूक नियमन आणि अन्नाची इच्छा कमी होते

स्वेन्जा मेयहोफर 1,2,3,4,†, रॉड्रिगो चामारो 1,5,†, मॅनफ्रेड हॉलश्मिड 2,6,7, डेनिसा स्पायरा 1, नेली क्लिन्समन 1, बर्न्ड शुल्टेस 1, हेंड्रिक लेहनेर्ट 4,8, सेबॅस्टियन एम मेयहोफर 1,2,4,*, ब्रिटा विल्म्स 1,2,4

संपादक: अल्बर्ट लेक्यूब, डेव्हिड जे मेला

Appetite Regulation and      Nutrients. 2023 Apr 23;15(9):2035. doi: 10.3390/nu15092035

Late, but Not Early, Night Sleep Loss Compromises Neuroendocrine Appetite Regulation and the Desire for Food

Svenja Meyhöfer 1,2,3,4,†, Rodrigo Chamorro 1,5,†, Manfred Hallschmid 2,6,7, Denisa Spyra 1, Nelli Klinsmann 1, Bernd Schultes 1, Hendrik Lehnert 4,8, Sebastian M Meyhöfer 1,2,4,*, Britta Wilms 1,2,4

Editors: Albert Lecube, David J Mela

          चर्चा

या संतुलित क्रॉसओव्हर प्रयोगात, आम्ही मानवांमध्ये भूक आणि खाण्याची इच्छा यांच्या नियमनावर झोप कमी होण्याच्या वेळेच्या परिणामांचा अभ्यास केला.

रात्री उशिरा झोप कमी झाल्यामुळे, परंतु रात्री लवकर झोप कमी झाल्यामुळे नाही, घ्रेलिनची पातळी, तसेच भूक आणि खाण्याची इच्छा वाढल्याचे दिसून आले.

आणि त्यानंतरच्या सकाळी खाण्याची इच्छा वाढल्याचे निरीक्षण नोंदवले गेले, याउलट लेप्टिनच्या पातळीवर केवळ झोपेच्या तीव्र कमतरतेचा किंवा झोप कमी होण्याच्या वेळेचा कोणताही परिणाम झाला नाही. आमचा डेटा दर्शवितो की रात्रीच्या पूर्वार्धात झोप कमी करण्याच्या तुलनेत, रात्रीच्या उत्तरार्धात झोप कमी केल्यास घ्रेलिन, भूक, खाण्याची इच्छा आणि खाण्याच्या इच्छेवर झोपेच्या तीव्र कमतरतेचा अधिक स्पष्ट परिणाम होतो.

हे मानवी खाण्याच्या इच्छेच्या नियमनामध्ये वेळेनुसार कमी होणाऱ्या झोपेच्या क्रोनोबायोलॉजिकल भूमिकेवर जोर देते.

प्लाझ्मा घ्रेलिन आणि लेप्टिनच्या पातळीवर झोपेच्या कमतरतेच्या (वेगवेगळ्या वेळेनुसार) परिणामांवरील अभ्यासातून विसंगत निष्कर्ष मिळाले आहेत. आमच्या गटात, ७ तासांच्या झोपेच्या रात्रीच्या तुलनेत, एका रात्रीच्या अपुऱ्या झोपेनंतर (२२:३० ते ०३:३० पर्यंत झोप) घ्रेलिनची पातळी वाढलेली दिसून आली [३५]. दुसऱ्या एका अभ्यासात असे दिसून आले की, १० तासांच्या रिकव्हरी झोपेच्या दोन रात्रींच्या तुलनेत, दोन रात्रींच्या अपुऱ्या झोपेमुळे (०१:०० ते ०५:०० पर्यंत झोप) निरोगी पुरुषांमध्ये लेप्टिनची पातळी कमी आणि घ्रेलिनची पातळी वाढली, आणि हे बदल त्यानंतरच्या दिवशी भूक आणि खाण्याची इच्छा वाढण्याशी संबंधित होते [२०].शिवाय, चार रात्री झोप कमी केल्याने (रात्री 01:00 ते 05:30 पर्यंत) लेप्टिनमध्ये कोणताही बदल न होता घ्रेलिनची पातळी वाढली, आणि घ्रेलिनच्या पातळीतील वाढ गोड पदार्थांमधून घेतलेल्या कॅलरीजशी संबंधित होती [17].

एकंदरीत, बहुतेक, पण सर्वच नाही [18] डेटा आमच्या अभ्यासाशी सुसंगत असल्याचे दिसते, जो रात्रीच्या उत्तरार्धात झोप कमी झाल्यास घ्रेलिनची पातळी वाढल्याचे दर्शवतो. वेगवेगळ्या अभ्यासांमधील घ्रेलिनच्या पातळीच्या मोजमापाच्या संदर्भात, हे लक्षात घेणे आवश्यक आहे की काही अभ्यासांनी एकूण घ्रेलिनबद्दल माहिती दिली, तर इतरांनी स्वतंत्रपणे अ‍ॅसिलेटेड आणि डीअ‍ॅसिलेटेड घ्रेलिनबद्दल माहिती दिली, जी अधिक माहितीपूर्ण ठरली असती. काही अभ्यासांमध्ये, घ्रेलिनमधील बदल वाढलेल्या ऊर्जा सेवनाशी देखील संबंधित होते [17,20],

जे रात्रीच्या दुसऱ्या भागात झोप कमी झाल्यानंतर भूकेच्या होमियोस्टॅटिक नियंत्रणात बदल झाल्याचे समर्थन करते. ब्रुसार्ड एट अल. सडपातळ पुरुषांमध्ये, साडेआठ तासांच्या चार रात्रींच्या झोपेच्या तुलनेत, साडेचार तासांच्या चार रात्रींच्या झोपेनंतर घ्रेलिनची पातळी आणि कॅलरी सेवनात ३०० किलोकॅलरीपेक्षा जास्त वाढ झाल्याचे नोंदवले गेले आहे. शिवाय, संध्याकाळच्या वेळी वाढलेली घ्रेलिनची पातळी ही जास्त ऊर्जा सेवनाशी संबंधित होती, जी प्रामुख्याने कर्बोदकांमुळे होती (१२). घ्रेलिन आणि लेप्टिन व्यतिरिक्त, पेप्टाइड वायवाय (PYY) किंवा ग्लुकागॉन-लाइक पेप्टाइड १ (GLP1) सारख्या ओरेक्सिजेनिक आणि एनोरेक्सिजेनिक ॲडिपोकाइन्सचे मापन, न्यूरोएंडोक्राइन भूक नियमनावर वेळेनुसार कमी झालेल्या झोपेच्या परिणामांचे सर्वसमावेशक मूल्यांकन करण्यासाठी समर्पक ठरेल.

आम्ही दाखवून दिले की, जेव्हा झोप कमी झाली, तेव्हा भूक आणि खाण्याची इच्छा वाढली, तसेच अन्नाची तीव्र इच्छाही वाढली, विशेषतः रात्रीच्या उत्तरार्धात. मॅकनील आणि इतर. १८ निरोगी तरुण पुरुष आणि स्त्रियांमध्ये [36] लवकर जागे होण्याच्या वेळेचा वापर करून (आमच्या 'उशिरा झोप कमी होणे' या स्थितीप्रमाणे) कमी केलेल्या झोपेचे (~४ तास) परिणाम, उशिरा झोपण्याच्या स्थितीच्या (आमच्या 'लवकर झोप कमी होणे' या स्थितीप्रमाणे) तुलनेत तपासले गेले. त्यांनी लवकर जागे होण्याच्या वेळेसह कमी झोपेनंतर उपाशीपोटी भूक आणि न्याहारीनंतरची भूक वाढल्याचे नोंदवले. याव्यतिरिक्त, नियंत्रित झोपेच्या स्थितीच्या तुलनेत लवकर जागे होण्याच्या वेळेसह कमी झोपेनंतर कमी चरबीयुक्त पदार्थांच्या तुलनेत उच्च चरबीयुक्त पदार्थांची स्पष्ट इच्छा आणि आवड वाढल्याचे दिसून आले [30]. दुसऱ्या एका अभ्यासात असे नोंदवले गेले की, ८ तासांच्या नियमित झोपेच्या तुलनेत, रात्रीच्या दुसऱ्या भागात (०२:०० ते ०६:०० वाजेपर्यंत) ४ तासांची झोप कमी केल्यावर ऊर्जेचे सेवन आणि जेवणापूर्वीची भूक वाढली [14].

मनोरंजक म्हणजे, हिबी आणि त्यांच्या सहकाऱ्यांनी [25] नोंदवल्याप्रमाणे, निरोगी पुरुषांमध्ये तीन दिवसांसाठी रात्री लवकर झोप कमी करण्याच्या प्रोटोकॉलचा (रात्री 03:30 पर्यंत जागे राहणे) वापर करून 3.5 तासांच्या झोपेच्या स्थितीमुळे भूक आणि संभाव्य अन्न सेवनात वाढ झाली. हे परिणाम आमच्या गटाच्या पूर्वीच्या निष्कर्षांच्या विरुद्ध आहेत, ज्यात असे दिसून आले आहे की रात्रीच्या पहिल्या अर्ध्या भागात (रात्री 02:45 पर्यंत जागे राहणे) दोन रात्रींची झोप कमी झाल्याने निरोगी मानवांमध्ये भूक, खाण्याची इच्छा आणि ऊर्जेच्या सेवनावर परिणाम झाला नाही [15]. यानुसार, आमचा सध्याचा डेटा देखील हिबी आणि त्यांच्या सहकाऱ्यांच्या अभ्यासाशी विसंगत आहे, कारण रात्री उशिरा झोप कमी होणे किंवा सामान्य झोपेच्या स्थितीच्या तुलनेत, रात्री लवकर झोप कमी झाल्याने घ्रेलिन किंवा भुकेच्या भावनेवर परिणाम झाला नाही. ही विसंगती - किमान अंशतः - अभ्यासाच्या वेगवेगळ्या कालावधीशी संबंधित असू शकते, आमच्या अभ्यासात अनुक्रमे एक आणि दोन रात्री, तर हिबी आणि त्यांच्या सहकाऱ्यांच्या अभ्यासात तीन रात्री. हे देखील नमूद करण्यासारखे आहे की असे मांडण्यात आले आहे की - पाश्चात्त्य वातावरणात - भूक आणि खाण्याच्या इच्छेच्या भावनांचे मूल्यांकन हे अन्न सेवनाच्या होमियोस्टॅटिक नियमनाऐवजी आनंददायी घटकाचे प्रतिबिंब दर्शवेल [36]. आमच्या डेटानुसार, सकाळी भूक आणि खाण्याच्या इच्छेच्या वाढलेल्या भावना (मुख्यतः रात्री उशिरा झोप कमी झाल्यानंतर) या दोन्ही झोप कमी होण्याच्या परिस्थितीनंतर सकाळी खाण्याच्या इच्छेच्या नियंत्रणाच्या वाढलेल्या आनंददायी घटकाशी संबंधित असू शकतात. तथापि, सकाळी वाढलेली घ्रेलिनची पातळी ही ऊर्जा सेवनाच्या नियमनाच्या होमियोस्टॅटिक घटकावर रात्री उशिरा झोप कमी होण्याच्या प्रतिकूल परिणामाचे प्रतिबिंब असू शकते.

इतरांनी देखील नियंत्रित झोपेच्या स्थितीच्या तुलनेत, लवकर जागे होण्याच्या वेळेसह कमी झोपेनंतर कमी चरबीयुक्त पदार्थांच्या तुलनेत उच्च-चरबीयुक्त पदार्थांसाठी वाढलेली स्पष्ट इच्छा आणि आवड दर्शविली आहे [30]. पदार्थांबद्दलची आवड आणि इच्छा या अन्न-बक्षिसाचे नियमन करणाऱ्या दोन स्वतंत्र प्रक्रिया आहेत [37]. आवड ही संवेदी आनंदाच्या अनुभवाचे प्रतिबिंब दर्शवते, तर इच्छा ही खाण्याच्या इच्छेशी संबंधित प्रेरणा आणि, पुढे सांगायचे झाल्यास, अन्न-बक्षिसाची प्रत्यक्ष इच्छा दर्शवते. कार्यात्मक इमेजिंग अभ्यासांद्वारे दर्शविल्याप्रमाणे, मेंदूच्या रचना खाण्याच्या इच्छेच्या नियंत्रणात वेगवेगळ्या प्रकारे सामील असतात. इच्छा-संबंधित प्रक्रिया व्हेंट्रल पॅलिडम आणि स्ट्रायटमशी संबंधित आहेत, तर आवड-विशिष्ट क्षेत्रे ऑर्बिटोफ्रंटल कॉर्टेक्स, इन्सुलर कॉर्टेक्स आणि अॅमिग्डाला आहेत, जे अन्न आणि अन्न-संबंधित संकेतांसाठी आवड आणि इच्छा यांच्या मज्जासंस्थेतील विलगतेकडे सूचित करते [38]. झोपेच्या कमतरतेच्या संदर्भात इच्छा/आवड प्रक्रियेचा विचार करताना, हे लक्षात घेणे महत्त्वाचे आहे की दिवसाची वेळ अन्नाच्या इच्छेवर परिणाम करते, परंतु आवडीवर नाही. आम्ही हे दाखवू शकलो की, मुक्त जीवनशैली आणि प्रयोगशाळेतील दोन्ही परिस्थितीत, ऊर्जा-दाट पदार्थांची आवड सकाळ आणि संध्याकाळी वेगळी नव्हती, तर इच्छा संध्याकाळी स्पष्टपणे वाढली होती, जरी भूक आणि तृप्तीची भावना तशीच राहिली [39]. तथापि, आमच्या सध्याच्या अभ्यासात, आवड आणि इच्छा यांचा विचार केला गेला नाही, ज्यामुळे विशेषतः वेळेनुसार झोपेच्या कमतरतेच्या संदर्भात, न्यूरोएंडोक्राइन भूक नियमनाबद्दल अधिक सखोल माहिती मिळू शकली असती.

दीर्घकालीन सर्केडियन व्यत्यय केवळ अपुऱ्या आणि कमी झोपेच्या वेळीच होत नाही, तर रोटेटिंग शिफ्ट वर्क किंवा (सामाजिक) जेटलॅग दरम्यान देखील होतो आणि त्यामुळे न्यूरोएंडोक्राइन भूक नियमनावर परिणाम होतो. सोशल जेटलॅग हा सर्केडियन लय विस्कळीत होण्याचा एक सामान्य प्रकार आहे आणि तो ७०% लोकसंख्येमध्ये आढळतो [९]. याची व्याख्या व्यक्तीचे अंतर्जात सर्केडियन घड्याळ आणि झोपेची प्रत्यक्ष वेळ यांच्यातील विसंगती म्हणून केली जाते [४०]. एका क्रॉस-सेक्शनल निरीक्षणात्मक अभ्यासात असे आढळून आले की, केवळ झोपेची कमतरता असलेल्या व्यक्तींच्या तुलनेत, सोशल जेटलॅग असलेल्या व्यक्तींमध्ये, झोपेच्या कमतरतेचा विचार न करताही, जास्त कॅलरीयुक्त अन्नाची भूक वाढलेली होती [४१]. याव्यतिरिक्त, सोशल जेटलॅग असलेल्या व्यक्तींमध्ये घ्रेलिनची पातळी वाढलेली होती. ही माहिती दर्शवते की सोशल जेटलॅगमुळे अन्नाचे प्रोत्साहन मूल्य वाढते, तसेच हे पदार्थ खाण्यातून मिळणाऱ्या अपेक्षित आनंदाचीही जाणीव होते. एका fMRI अभ्यासानुसार, त्याच कार्यगटाने असे नोंदवले की सोशल जेटलॅगचा संबंध आनंददायी आहाराशी, म्हणजेच रिवॉर्ड सिस्टीमशी संबंधित मेंदूच्या भागांमधील बदललेल्या विश्राम-स्थितीतील क्रियाकलापांशी आहे. सविस्तरपणे सांगायचे झाल्यास, सोशल जेटलॅग असलेल्या व्यक्तींमध्ये पुटामेनमध्ये वाढलेली क्रियाशीलता दिसून आली, जो स्ट्रायटमचा एक भाग असून त्याची कार्ये रिवॉर्ड सिस्टीमशी जोडलेली आहेत. महत्त्वाचे म्हणजे, हा परिणाम कमी झोपेच्या कालावधीवर अवलंबून नाही. शिवाय, सोशल जेटलॅग असलेल्या व्यक्तींनी उच्च कॅलरीयुक्त अन्नाची जास्त भूक असल्याचे सांगितले आणि सोशल जेटलॅग नसलेल्या व्यक्तींपेक्षा त्यांच्या खाण्याच्या सवयी एकूणच हानिकारक होत्या [42].

 अशाप्रकारे, डेटा या पुराव्यास समर्थन देतो की सोशल जेटलॅग असलेल्या व्यक्तींना आनंदासाठी खाण्याची (हेडोनिक फीडिंग) आणि दीर्घकाळात शरीराचे वजन वाढण्याची शक्यता असते.

झोपेच्या तीव्र कमतरतेच्या परिस्थितीत, प्रायोगिक अभ्यासांनुसार रात्रीच्या कॅलरीजमुळे कॅलरी सेवनात वाढ झाल्याचे दिसून येते. दुसरीकडे, उंदीर आणि मानव या दोघांमध्येही असे दिसून आले आहे की, रोटेटिंग शिफ्ट वर्क पॅराडाइम [43] करत असताना सामान्य जेवणाच्या वेळी खाणे, किंवा दीर्घकालीन झोपेच्या कमतरतेखाली असताना कॅलरी गरजेनुसार कॅलरी सेवन करणे [44], या दोन्हीमुळे सर्केडियन लय बदलली नाही. दुसऱ्या अभ्यासात, सहभागींना ३२-दिवसांच्या इनपेशंट प्रोटोकॉलमध्ये ठेवण्यात आले होते, ज्यात झोपेच्या कमतरतेसह किंवा त्याशिवाय २० तासांच्या फोर्स्ड डिसिंक्रोनी प्रोटोकॉलच्या २४ सायकल्सचा समावेश होता. भुकेच्या व्यक्तिनिष्ठ भावनांवर कमी झोपेचा कोणताही परिणाम लक्षात येण्यासारखा नव्हता, कारण भुकेची लय संध्याकाळी उच्चांक आणि पहाटेच्या वेळी कमी पातळीसह स्थिर राहिली, जसे की शीर आणि त्यांच्या सहकाऱ्यांनी [45] आधीच दाखवले आहे. तथापि, दीर्घकालीन सर्केडियन लय विस्कळीत होणे हे झोपेच्या कालावधीपासून स्वतंत्रपणे, भुकेच्या व्यक्तिनिष्ठ भावना कमी होण्याशी संबंधित होते. हा अभ्यास दीर्घकालीन सर्केडियन विस्कळीतपणा आणि अपुऱ्या झोपेच्या वेगवेगळ्या योगदानांबद्दल अधिक सखोल माहिती देतो आणि असे सुचवतो की अपुऱ्या झोपेचा व्यक्तिनिष्ठ भुकेवर होणारा परिणाम काही अभ्यासांनी [20,35] नोंदवलेल्या परिणामापेक्षा कमी तीव्र असतो, परंतु सर्व अभ्यासांनी नाही [15]. दीर्घकालीन सर्केडियन विस्कळीतपणाच्या संदर्भात झोप कमी होण्याच्या वेळेच्या वेगळ्या परिणामांचे मूल्यांकन करण्यासाठी येथे पुढील अभ्यासांची आवश्यकता आहे, कारण असा अंदाज लावला जाऊ शकतो की अपुऱ्या झोपेचे क्रोनोबायोलॉजिकल पैलू भुकेच्या जाणिवेवर वेगळ्या प्रकारे—किमान अंशतः—परिणाम करतात, जसे की आमच्या सध्याच्या अभ्यासात दिसून आले आहे.

आम्ही ८ तासांच्या नियंत्रक झोपेच्या तुलनेत, केवळ एका रात्री चार तासांची झोप कमी केल्यानंतर भूक नियमन आणि अन्नाची इच्छा यांचे मूल्यांकन केले. त्यामुळे, आम्ही दीर्घकाळ टिकणाऱ्या झोपेच्या कमतरतेच्या परिणामांबद्दल किंवा दुसरीकडे, झोपेच्या बदललेल्या वेळेबद्दल, तसेच सोशल जेटलॅगबद्दल कोणताही निष्कर्ष काढू शकत नाही. झोपेच्या वेळेत बदल करून झोपेच्या कमतरतेच्या दीर्घकालीन परिणामांचे मूल्यांकन करण्यासाठी पुढील अभ्यासांची आवश्यकता आहे, उदा., फोर्स्ड डिसिंक्रोनी प्रोटोकॉल [44] वापरून. तथापि, शिफ्ट वर्क पॅराडाइम (उदा.,) वापरून प्राण्यांवर अभ्यास करण्याच्या तुलनेत, प्रायोगिक परिस्थितीत मानवांवर असे अभ्यास करण्याची शक्यता मर्यादित आहे. आणखी एक मर्यादा म्हणजे, आमच्या अभ्यास गटात तरुण, निरोगी आणि सामान्य वजनाचे पुरुष समाविष्ट होते. जरी आम्हाला लिंगभेदाची अपेक्षा नसली तरी, आम्ही स्त्रियांवर दिसून आलेले परिणाम लागू करू शकत नाही. खरं तर, झोपेच्या कमतरतेच्या चयापचय परिणामांबद्दलचे सध्याचे पुरावे बहुतेक पुरुषांवर केलेल्या अभ्यासातून मिळाले आहेत. तथापि, तरुण निरोगी प्रौढ, पुरुष आणि स्त्रिया दोघांच्याही अभ्यासात भूक, खाण्याची इच्छा, ऊर्जेचे सेवन आणि अन्नाच्या उत्तेजनांना प्रतिसाद देण्याची क्षमता [46] यामध्ये सातत्यपूर्ण वाढ झाल्याचे, तसेच तरुण प्रौढांमध्ये इन्सुलिन संवेदनशीलता कमी झाल्याचे [19] नोंदवले गेले आहे. महत्त्वाची गोष्ट म्हणजे, त्या अभ्यासांमध्ये झोप कमी करण्याच्या उपायांचा कालावधी वेगवेगळा वापरण्यात आला आहे. महिलांमध्ये, तीव्र स्वरूपाच्या आंशिक झोपेच्या निर्बंधानंतर (३ तासांची झोप) सकाळच्या लेप्टिनच्या पातळीत वाढ झाल्याचे दिसून आले आहे [२२,४७], परंतु भुकेच्या गुणांकात कोणताही बदल झालेला नाही [२२]. जास्त कालावधीच्या उपायांनंतर (चार रात्री), निरोगी महिलांमध्ये आंशिक झोपेच्या निर्बंधानंतर ऊर्जेचे सेवन वाढल्याचे आणि वजन वाढल्याचे नोंदवले गेले आहे [१३]. इतर अभ्यासांमध्ये, पुरुष आणि महिलांमधील झोप कमी होण्याच्या परिणामांची तुलना करताना, केवळ पुरुषांमध्येच ४-तासांच्या झोपेच्या निर्बंधानंतर चार दिवसांनी घ्रेलिनच्या पातळीत वाढ झाल्याचे दिसून आले आहे [४८]. याव्यतिरिक्त, पाच दिवस ४ तासांच्या झोपेनंतर (सकाळी ०४:०० ते ०८:०० पर्यंत झोप), पुरुषांमध्ये, परंतु महिलांमध्ये नाही, एकूण आणि रात्री उशिराच्या वेळेतील ऊर्जेचे सेवन वाढल्याचे दिसून आले [४९]. तथापि, हे शेवटचे अभ्यास आमच्या सध्याच्या अभ्यासाशी तुलना करण्यायोग्य नाहीत, कारण आम्ही अत्यंत तीव्र (एका रात्रीसाठी) झोप कमी करण्याच्या उपायांचे मूल्यांकन केले. हे देखील नमूद करणे महत्त्वाचे आहे की, सहभागींची संख्या कमी असूनही, पॅरामीट्रिक चाचणी प्रक्रिया वापरली गेली. गोलाकारपणाची समस्या सोडवण्यासाठी, आम्ही ग्रीन हाऊस गेसर पद्धतीचा वापर केला. शिवाय, आमचे निष्कर्ष चयापचय रोगांना बळी पडणाऱ्या व्यक्तींमध्ये, जसे की लठ्ठपणा आणि टाईप २ मधुमेह (T2D) असलेल्या रुग्णांमध्ये, सत्यापित केले पाहिजेत. वर चर्चा केल्याप्रमाणे, अन्न सेवनाच्या नियमनाचे मूल्यांकन करण्यासाठी अधिक व्यापक पद्धती, जसे की 'वॉन्टिंग/लायकिंग टास्क' किंवा fMRI, वापरल्यास अपुऱ्या झोपेचा आणि तिच्या वेळेचा अन्नाच्या इच्छेवरील परिणामाबद्दल अधिक सखोल माहिती मिळेल.

Late Night sleep loss

      Nutrients. 2023 Apr 23;15(9):2035. doi: 10.3390/nu15092035

Late, but Not Early, Night Sleep Loss Compromises Neuroendocrine Appetite Regulation and the Desire for Food

Svenja Meyhöfer 1,2,3,4,†, Rodrigo Chamorro 1,5,†, Manfred Hallschmid 2,6,7, Denisa Spyra 1, Nelli Klinsmann 1, Bernd Schultes 1, Hendrik Lehnert 4,8, Sebastian M Meyhöfer 1,2,4,*, Britta Wilms 1,2,4

Editors: Albert Lecube, David J Mela

    Discussion

In this balanced crossover experiment, we examined the effects of the timing of sleep loss on the regulation of hunger and appetite in humans.

 ‘Late-night sleep loss’, but not ‘early-night sleep loss’, elevated ghrelin concentrations, as well as feelings of hunger and appetite, 

and desire for food during the subsequent morning was observed, whereas leptin concentrations were not affected by acute sleep loss per se nor timing of sleep loss. Our data show a more pronounced effect of acute sleep loss on ghrelin, hunger, appetite, and the desire to eat when sleep is restricted in the second half of the night compared to a restriction of sleep during the first half of the night.

 This underscores the chronobiological role of timed sleep loss in human appetite regulation.

Studies on the effects of sleep restriction (with different timing) on plasma ghrelin and leptin levels have yielded inconsistent results. Our group showed increased ghrelin levels after one night of partial sleep restriction (sleep from 22:30 to 03:30 h) compared to a night with 7 h of sleep [35]. Another study showed that two nights of sleep restriction (sleep from 01:00 to 05:00 h), as compared to two nights with 10 h recovery sleep, resulted in lower leptin and higher ghrelin levels in healthy men, and these changes were associated with increased feelings of hunger and appetite during the subsequent day [20]. 

Furthermore, four nights of sleep restriction (from 01:00 to 05:30 h) increased ghrelin levels with no changes in leptin, and the increase in ghrelin levels correlated with ingested calories from sweet foods [17]. 

Overall, most, but not all [18] data, seem to be aligned with our study, which shows elevated ghrelin levels when sleep loss occurs in the late part of the night. With regard to the measurement of ghrelin levels within the different studies, one needs to point out that some studies reported on total ghrelin, whereas others reported on acylated and deacylated ghrelin, separately, which would have been more informative. In some studies, changes in ghrelin were also correlated with increased energy intake [17,20], 

supporting altered homeostatic control of appetite after sleep loss during the second half of the night. Broussard et al. reported on increased ghrelin levels and caloric intake by more than 300 kcal after four nights of 4.5 h sleep compared to four nights of 8.5 h sleep in lean men. Furthermore, elevated ghrelin levels in the evening were related to higher energy intake, mainly due to carbohydrates (12). Besides ghrelin and leptin, measurements of orexigenic and anorexigenic adipokines, such as Peptide YY (PYY) or Glucagon-like peptide 1 (GLP1), would be relevant to comprehensively assess the effects of timed sleep loss on neuroendocrine appetite regulation.

We showed elevated feelings of hunger and appetite, as well as desire for food, when sleep was restricted, again, in the late part of the night. McNeil et al. evaluated the effects of shortened sleep (~4 h) using an advanced wake time (similar to our ‘late sleep loss’ condition) vs. a delayed bedtime condition (similar to our ‘early sleep loss’ condition) in 18 healthy young men and women [36]. They reported higher fasting appetite and post-breakfast ratings after short sleep with the advanced wake time. Additionally, increased explicit wanting and liking for high-fat relative to low-fat foods after short sleep was observed with advanced wake time vs. the control sleep condition [30]. Another study reported increased energy intake and pre-prandial hunger levels upon one night of 4 h sleep restriction during the second half of the night (from 02:00–06:00 h), as compared to 8 h of regular sleep [14].

Interestingly, a 3.5 h sleep condition using an early night sleep loss protocol (wake until 03:30 h) for three days in healthy men increased hunger and prospective food consumption, as reported by Hibi and co-workers [25]. These results contrast with previous findings from our group, showing that two nights of sleep loss during the first half of the night (wake until 02:45 h) did not affect feelings of hunger and appetite and energy intake in healthy humans [15]. In line with this, our present data also disagree with the study by Hibi et al., as early night sleep loss did not affect ghrelin or hunger feelings compared with late night sleep loss or a control sleep condition. This discrepancy could be related—at least partly—to the different study duration, one and two nights, respectively, in our studies vs. three nights in the study by Hibi and co-workers. It is also worth mentioning that it has been proposed that—in Westernized settings—the assessment of hunger and appetite feelings would reflect the hedonic component, rather than the homeostatic regulation of food intake [36]. Our data showed increased hunger and appetite feelings in the morning (mainly after late night sleep loss) could relate to exacerbated hedonic component of appetite control in the morning after both sleep loss conditions. However, the increased morning ghrelin levels could reflect the adverse effect of a late-night sleep loss for the homeostatic component of energy intake regulation.

Other have also shown increased explicit wanting and liking for high-fat relative to low-fat foods after short sleep with advanced wake time vs. a control sleep condition [30]. Liking and wanting for foods are two separate processes modulating food reward [37]. Whereas liking mirrors the sensory pleasure experience, wanting reflects the motivation related to appetite and, putting forward, the actual desire for food reward. Cerebral structures are differently involved in appetite control, as shown by functional imaging studies. Wanting-related processes are related to ventral pallidum and striatum, whereas liking specific regions are the orbitofrontal cortex, insular cortex, and amygdala, which hints at a neural dissociation of liking and wanting for foods and food-related cues [38]. When addressing the wanting/liking process in the context of sleep restriction, it is relevant to consider that time of day impacts wanting, but not liking, for food. We could show that, both under free living conditions and laboratory settings, liking for energy-dense foods was not different in the morning and evening, whereas wanting was clearly increased in the evening, albeit feelings of hunger and satiety remained unchanged [39]. In our present study, however, liking and wanting were not addressed, which would have allowed for a closer insight into the neuroendocrine appetite regulation, especially in the context of timed sleep loss.

Chronic circadian disruption not on only occurs during insufficient and short sleep, but also during rotating shift work or (social) jetlag and, thus, affects neuroendocrine appetite regulation. Social jetlag is a common form of circadian rhythm disruption and presents in up to 70% of the population [9]. It is defined as the misalignment between individual’s endogenous circadian clock and the actual sleep time [40]. One cross-sectional observational study reported elevated appetite for caloric-dense food in subjects with social jetlag, independent of sleep deprivation compared with subjects with sleep deprivation alone [41]. In addition, ghrelin levels were elevated in those with social jet lag. These data point to a social jetlag-related increase in incentive value of food, together with anticipated pleasure of ingesting these foods. Upon a fMRI study, the same workgroup reported that social jetlag is associated with altered resting-state activity in brain regions related to hedonic feeding, i.e., the reward system. In detail, an increased activity in the putamen, part of the striatum with functions linked to the reward system, was shown in subjects with social jetlag. Importantly, this effect is independent of short sleep duration. Further, subjects with social jetlag reported a higher perceived appetite for high caloric food and had overall detrimental eating habits than those without social jetlag [42]. Thus, data support evidence that subjects with social jetlag are prone to hedonic feeding and, in the long term, to body mass gain.

Under an acute sleep restriction setting, experimental studies report on increased caloric intake due to night-time calories. On the other hand, it has been shown, both in mice and humans, that feeding either at normal eating time while performing a rotating shift work paradigm [43], or having caloric intake matched for the caloric needs while under chronic sleep restriction [44], did not alter circadian rhythms. In the latter study, subjects were exposed to a 32-day inpatient protocol, including 24 cycles of a 20 h forced desynchrony protocol either with or with sleep restriction. There was no impact of short sleep in subjective feelings of hunger that was detectable because hunger rhythm remained stable with a peak in the evening and low levels in the early morning, as already shown by Scheer et al. [45]. Chronic circadian disruption, however, was associated with decreased subjective feelings of hunger, independent of the sleep duration. This study provides deeper insight into the different contributions of chronic circadian disruption per se and short sleep and suggested a less strong impact of short sleep on subjective hunger than reported by some studies [20,35], but not all [15]. Further studies are needed here to evaluate the distinct effects of timing of sleep loss in the context of chronic circadian disruption, since one may speculate that the chronobiological aspects of short sleep differently—at least in part—affects feeling of hunger, as shown in our present study.

We assessed appetite regulation and desire for food after only one night of sleep restriction by four hours compared to control sleep of 8 h. Therefore, we cannot draw any conclusions concerning the effects of longer-lasting sleep restriction or, on the other hand, shifted sleep, as well as social jetlag. Further studies are needed to evaluate the prolonged effects of sleep restriction with altered sleep timing, e.g., using a forced desynchrony protocol [44]. However, the possibility to perform such studies in humans under experimental settings is limited compared to conducting an animal study using a shift work paradigm (e.g.,). As a further limitation, our study population included young, healthy, and normal-weight men. Although we do not expect gender differences, we cannot extrapolate the observed effects on women. In fact, current evidence regarding the metabolic consequences of sleep restriction has been provided from studies conducted mostly in men. However, studies comprising young healthy adults, both men and women, have reported consistent increases in hunger, appetite, energy intake, and susceptibility to food stimuli [46], together with reduced insulin sensitivity, in young adults [19]. Importantly, those studies have used different duration of sleep loss intervention. In females, increased morning leptin levels [22,47], but no changes in hunger scores, have been shown after an acute partial sleep restriction (3 h of sleep) [22]. With longer duration of intervention (four nights), increased energy intake and weight gain have been reported after partial sleep restriction in healthy women [13]. Others, comparing the effects of sleep loss in men and women, have shown increased ghrelin levels after four days of sleep restricted to 4-h only in men [48]. Additionally, after five days of 4 h of sleep (sleep from 04:00 to 08:00 h), men, but not women, showed exacerbated overall and late-night hour energy intake [49]. These last studies, however, are not comparable to our current study, as we assessed a very acute (one night) sleep loss intervention. It is further important to point out that, despite the small number of participants, a parametric test procedure was used. To address sphericity, we used the Green House Geisser approach. Moreover, our results should be confirmed in subjects prone to metabolic diseases, such patients as with obesity and T2D. As discussed above, using more comprehensive methods to assess the regulation of food intake, such as the wanting/liking task, or fMRI, would provide deeper insight into the impact of short sleep and its timing

Night sleep loss and desire for food

 

Nutrients. 2023 Apr 23;15(9):2035. doi: 10.3390/nu15092035

Late, but Not Early, Night Sleep Loss Compromises Neuroendocrine Appetite Regulation and the Desire for Food

Svenja Meyhöfer 1,2,3,4,†, Rodrigo Chamorro 1,5,†, Manfred Hallschmid 2,6,7, Denisa Spyra 1, Nelli Klinsmann 1, Bernd Schultes 1, Hendrik Lehnert 4,8, Sebastian M Meyhöfer 1,2,4,*, Britta Wilms 1,2,4

Editors: Albert Lecube, David J Mela

 Introduction

Sleep loss has become common in modern societies [1] 

and has been reported in different populations and age groups during the past decades [2].

 In parallel, the prevalence of obesity and metabolic comorbidities, such as type 2 diabetes (T2D), are rising worldwide [3].

 A meta-analysis, including more than 600,000 adults and 30,000 children, showed a strong association between reduced sleep duration of less than 5 h/day and obesity [4].

 Large epidemiological studies indicate that reduced quantity and decreased sleep quality are associated with adverse metabolic conditions, such as obesity and impaired glucose tolerance, and several meta-analyses confirmed an association between short, but also long, sleep and the prevalence of the metabolic syndrome [5,6]. 

An important mediator for these metabolic changes seems to be changes in the central nervous control of energy homeostasis, including an increase in appetite, sensitivity to food stimuli, and energy intake. Thus, sleep loss seems to be a relevant risk factor for metabolic diseases, such as obesity and T2D [7].

 As sleep is a process regulated by the circadian clock, being related to the suprachiasmatic nucleus of the hypothalamus as the main zeitgeber and also feedback to the clock [8],

 the consequences of impaired sleep duration and timing can lead to acute, but also chronic, circadian disruption. In fact, the detrimental health effects of mistimed sleep have been shown by adverse health effects of shift work and social jetlag, two widespread conditions in current societies [9,10,11]. 

A meta-analysis, including 13 studies, revealed that night shift work is associated with a 57% increased risk of the metabolic syndrome. Data further showed a dose–response relationship with years of night shift work, with 77% increased risk of metabolic syndrome in those with longer exposure to shift work than in those with shorter work in rotating shift (12%) [12].

Most experimental studies have shown that acute sleep loss increases ghrelin and decreases leptin concentrations, as relevant orexigenic and anorexigenic hormonal mediators of hunger and appetite, respectively. In line, short sleep was accompanied by increased feelings of hunger and appetite, as well as caloric intake [13,14],

 which could promote weight gain and obesity in long term. However, there are also data on unchanged hunger, appetite, and food intake after acute sleep loss [15].

 This, at first glance, seems to be a contradictory result, but it may be able to be explained—at least in part—by overeating after both short and regular sleep, since subjects had unlimited access to different foods, including tasty and high caloric items in this last study with ingested energy exceeding the calculated 24 h energy requirement by approximately 60% [15].

The mechanisms linking short sleep to acute changes in feelings of hunger and, thus, shift in the energy balance are under investigation. Elevated ghrelin concentrations might mediate increased food intake, and some, but not all, studies report increased ghrelin concentrations after shortened sleep [16,17,18,19].

 In addition, dampened leptin concentrations trigger increased food intake after sleep restriction in some studies [20,21]. 

However, others have reported unchanged or elevated leptin concentrations after varying degrees of shortened sleep [16,22,23].

 Different study protocols could partly explain these contradictory results regarding the degree and duration of sleep restriction, access to food (e.g., unlimited vs. served according to subject’s energy requirement), type of foods (e.g., palatable vs. standard), participants’ characteristics, and physical activity level.

Regarding the desire to eat after short sleep, some studies report no changes in perceived pleasantness of food or the desire to eat after one night with reduced sleep of 4 h and after five consecutive days of insufficient sleep, mimicking a work week, respectively [14,24].

 In contrast, others have shown increased hunger and prospective food consumption after three nights of sleep restriction with a sleep duration of 3.5 h per night [25].

 Since most studies did not synchronize sleeping and waking periods under experimental conditions, it has been speculated [15] that the waking time is a prerequisite for the orexigenic effect of sleep loss [14,26,27].

The impact of sleep timing, irrespective of its duration and on the regulation of hunger and appetite, is less clear. Alterations in the timing of sleep during restricted sleep could result in dissimilar sleep and metabolic impairments, given the notorious influence of sleep on metabolic processes [7]. 

Early evidence on this issue showed that mistimed sleep (i.e., early night and late-night sleep loss) during restricted sleep led to changes in sleep architecture in young adults, even without differences in the anorectic hormone leptin levels between sleep restriction-timing conditions [28]. Others have reported that changes in sleep stages after sleep restriction (4 h sleep, from 01:00–05:00 h) was related to changes in hunger feelings [29]. McNeil et al. also showed increased appetite before and after breakfast after short sleep with advanced wake time (i.e., 4 h of sleep with advanced wake up time) in young adults [30]. The same group showed that short sleep with delayed wake-up time increased energy intake from carbohydrates [31]. Additionally, short sleep with both delayed bedtime and advanced wake-up time affected physical activity pattern.

We have previously shown that the timing of sleep loss is relevant for glucose homeostasis and physical activity patterns in healthy humans. Sleep loss, with advanced awakening time, led to reduced glucagon and altered cortisol levels [32] toand also led to reduced physical activity and intensity the day after [33].

 Thus, besides its consequences on sleep and metabolic outcomes, impairment in the control of appetite regulation can be expected after mistimed sleep loss.

The present study investigated the impact of the specific timing of sleep loss compared to regular sleep on appetite regulation and desire for foods. We hypothesized that both short sleep duration per se and the timing of sleep loss, i.e., early night sleep loss vs. late night sleep loss, may modulate the adverse effects of sleep loss on humans’ appetite regulation, feelings of hunger, and desire for food.

झोपेचा कालावधी कमी झाल्यामुळे भूक, खाण्याची इच्छ वाढते,

 संदर्भ

पोषक तत्वे. 2023 एप्रिल 23; 15(9): 2035. doi: 10.3390/nu15092035

रात्री उशिरा झोप कमी झाल्यास, पण लवकर झोप कमी न झाल्यास, न्यूरोएंडोक्राइन भूक नियमन आणि अन्नाची इच्छा कमी होते

स्वेन्जा मेयहोफर 1,2,3,4,†, रॉड्रिगो चामारो 1,5,†, मॅनफ्रेड हॉलश्मिड 2,6,7, डेनिसा स्पायरा 1, नेली क्लिन्समन 1, बर्न्ड शुल्टेस 1, हेंड्रिक लेहनेर्ट 4,8, सेबॅस्टियन एम मेयहोफर 1,2,4,*, ब्रिटा विल्म्स 1,2,4

संपादक: अल्बर्ट लेक्यूब, डेव्हिड जे मेला

Nutrients. 2023 Apr 23;15(9):2035. doi: 10.3390/nu15092035

Late, but Not Early, Night Sleep Loss Compromises Neuroendocrine Appetite Regulation and the Desire for Food

Svenja Meyhöfer 1,2,3,4,†, Rodrigo Chamorro 1,5,†, Manfred Hallschmid 2,6,7, Denisa Spyra 1, Nelli Klinsmann 1, Bernd Schultes 1, Hendrik Lehnert 4,8, Sebastian M Meyhöfer 1,2,4,*, Britta Wilms 1,2,4

Editors: Albert Lecube, David J Mela

सारांश

उद्दिष्ट: असे पुरावे आहेत की झोपेचा कालावधी कमी झाल्यामुळे भूक, खाण्याची इच्छा आणि अन्नसेवन वाढते,

ज्यामुळे टाइप २ मधुमेह आणि लठ्ठपणा यांसारखे चयापचयाचे आजार होतात. तथापि, झोपेच्या वेळेचा, तिच्या कालावधीचा विचार न करता, भूक आणि खाण्याची इच्छा यांच्या नियमनावरील परिणाम कमी स्पष्ट आहे.

रात्रीच्या उत्तरार्धात विरुद्ध पूर्वार्धात झोप कमी झाल्याने भूक, खाण्याची इच्छा आणि अन्नाची इच्छा यांच्या नियमनावर होणाऱ्या परिणामाचे मूल्यांकन करणे, हे आमचे उद्दिष्ट होते.

पद्धती: पंधरा सामान्य वजनाच्या ([सरासरी ± मानक त्रुटी] बॉडी-मास इंडेक्स: २३.३ ± ०.४ किलोग्रॅम/मीटर²) निरोगी पुरुषांचा यादृच्छिक, संतुलित, क्रॉसओव्हर डिझाइनमध्ये अभ्यास करण्यात आला. यामध्ये झोप कमी होण्याच्या दोन स्थितींचा समावेश होता, म्हणजेच, रात्रीच्या पहिल्या अर्ध्या भागात ४ तासांची झोप ('रात्री उशिरा झोप कमी होणे'), रात्रीच्या दुसऱ्या अर्ध्या भागात ४ तासांची झोप ('रात्री लवकर झोप कमी होणे'), आणि अनुक्रमे ८ तासांच्या झोपेसह एक नियंत्रण स्थिती ('नियमित झोप'). भूक आणि खाण्याची इच्छा व्हिज्युअल अॅनालॉग स्केलद्वारे तपासण्यात आली, आणि रात्रीच्या झोपेपूर्वी, झोपेदरम्यान आणि झोपेनंतर घेतलेल्या रक्ताच्या नमुन्यांमधून प्लाझ्मा घ्रेलिन आणि लेप्टिन मोजण्यात आले. निष्कर्ष: रात्री उशिरा झोप कमी झाल्यामुळे घ्रेलिन आणि भूक लागण्याची भावना, तसेच अन्नाची इच्छा वाढली, परंतु रात्री लवकर झोप कमी झाल्यामुळे असे झाले नाही, तर लेप्टिनवर झोप कमी होण्याच्या वेळेचा कोणताही परिणाम झाला नाही. निष्कर्ष: आमच्या माहितीनुसार, झोपेच्या कमतरतेची वेळ निरोगी पुरुषांमध्ये घ्रेलिन आणि भूकेच्या नियमनावर झोपेच्या तीव्र कमतरतेच्या परिणामांना नियंत्रित करते.

रात्री उशिरा झोप कमी होणे हे लठ्ठपणा आणि टाईप २ मधुमेह यांसारख्या चयापचय रोगांसाठी एक धोकादायक घटक असू शकते. त्यामुळे, आमचे निष्कर्ष क्रोनोबायोलॉजिकल झोपेच्या वेळेचे चयापचयविषयक महत्त्व अधोरेखित करतात.

Redduced sleep duration increases hunger appetite

 Nutrients. 2023 Apr 23;15(9):2035. doi: 10.3390/nu15092035

Late, but Not Early, Night Sleep Loss Compromises Neuroendocrine Appetite Regulation and the Desire for Food

Svenja Meyhöfer 1,2,3,4,†, Rodrigo Chamorro 1,5,†, Manfred Hallschmid 2,6,7, Denisa Spyra 1, Nelli Klinsmann 1, Bernd Schultes 1, Hendrik Lehnert 4,8, Sebastian M Meyhöfer 1,2,4,*, Britta Wilms 1,2,4

Editors: Albert Lecube, David J Mela

Abstract

Objective: There is evidence that reduced sleep duration increases hunger, appetite, and food intake,

 leading to metabolic diseases, such as type 2 diabetes and obesity. However, the impact of sleep timing, irrespective of its duration and on the regulation of hunger and appetite, is less clear. 

We aimed to evaluate the impact of sleep loss during the late vs. early part of the night on the regulation of hunger, appetite, and desire for food. 

Methods: Fifteen normal-weight ([mean ± SEM] body-mass index: 23.3 ± 0.4 kg/m2) healthy men were studied in a randomized, balanced, crossover design, including two conditions of sleep loss, i.e., 4 h sleep during the first night-half (‘late-night sleep loss’), 4 h sleep during the second night-half (‘early-night sleep loss’), and a control condition with 8h sleep (‘regular sleep’), respectively. Feelings of hunger and appetite were assessed through visual analogue scales, and plasma ghrelin and leptin were measured from blood samples taken before, during, and after night-time sleep. Results: Ghrelin and feelings of hunger and appetite, as well as the desire for food, were increased after ‘late-night sleep loss’, but not ‘early-night sleep loss’, whereas leptin remained unaffected by the timing of sleep loss. Conclusions: Our data indicate that timing of sleep restriction modulates the effects of acute sleep loss on ghrelin and appetite regulation in healthy men. 

‘Late-night sleep loss’ might be a risk factor for metabolic diseases, such as obesity and type 2 diabetes. Thereby, our findings highlight the metabolic relevance of chronobiological sleep timing.

Egg Consumption and Dementia

 

Association between Egg Consumption and Dementia in Chinese Adults.

Igbinigie PO, Chen R, Tang J, Dregan A, Yin J, Acharya D, Nadim R, Chen A, Bai Z, Amirabdollahian F.Nutrients. 2024 Oct 1;16(19):3340. doi: 10.3390/nu16193340.

Discussion

Our population-based case-control study examined the association between egg consumption and dementia. This study demonstrated that the odds of dementia increased with decreased consumption of eggs from Daily to Weekly to Monthly, while the odds of dementia in those consuming eggs ≥ Twice a day or those who were Non-consuming/<monthly were not significantly increased or reduced. Such an inverse association between egg consumption and dementia was independent of important confounding factors, including age, educational level, smoking, dietary intake of red meats, poultry, fish, vegetables and fruits and co-morbidities.

Despite the current literature lacking research on egg consumption associated with dementia, several studies have investigated the association with cognitive decline or impairment (CI) in older people [15,16,17,18,19,20]. An et al. [20] analysed data from 2816 older adults aged 60 years or older from the National Health and Nutrition Examination Survey (NHANES) 2011–2012 and 2013–2014 waves. Cognitive assessments included the Consortium to Establish a Registry for Alzheimer’s Disease Word List Learning Test (CERAD-WL), Word List Recall Test (CERAD-DR), Animal Fluency Test (AF) and Digit Symbol Substitution Test (DSST). Their findings indicated that neither the consumption status of whole eggs nor the quantity consumed daily was associated with cognitive test scores in older adults. However, other studies [16,17,29] have shown that the consumption of eggs could be beneficial for cognitive functioning. Sukik et al. [17] examined data from 4852 participants aged 55 years or older from the China Health and Nutrition Survey (CHNS). The CHES study collected data on dietary egg intake for each participant through 24-h dietary recalls over 3 consecutive days during home visits between 1991 and 2006 and assessed the cognitive function of the participants in 1997, 2000, 2004 and 2006. The authors found that egg intake was positively associated with global cognitive function, and in fully adjusted models, the regression coefficients across the quartiles of egg intake were 0, 0.11 (95% CI −0.28–0.51), 0.79 (95% CI 0.36–1.22) and 0.92 (95% CI 0.43–1.41), respectively. Compared to non-consumers, those with higher egg consumption (4th quartile) had an adjusted OR of 0.93 (0.74–1.19) for self-reported poor memory and 0.84 (0.69–1.02) for self-reported memory decline, both being not statistically significant. Kritz-Silverstein and Bettencourt [16] analysed data from a cohort of 617 men and 898 women aged 60 and older from the Rancho Bernardo Cohort, who were followed for 16.3 years. They found that egg intake at baseline was significantly associated with better cognitive function measured at follow-up in men (performance on Buschke total (p = 0.04), long-term (p = 0.02) and short-term (p = 0.05) recall but not in women (p-values > 0.05). Li et al. [29] examined data from a cohort of 9028 participants aged ≥ 60 years from the Zhejiang Ageing and Health Cohort Study without cognitive impairment at baseline and followed up for 6 years with three waves of measurements using the Mini-Mental State Examination (MMSE) for CI. The authors used log-binomial regression models for repeated measures with the Generalized Estimating Equations (GEE) method to assess the longitudinal effect of egg consumption on the risk of cognitive impairment. The authors found that participants who increased egg consumption had a reduced relative risk (RR) of CI compared to non-consumers or those who consumed eggs less than Weekly; the multiple adjusted RR of CI was 0.82 (0.76–0.89) for participants consuming 0.1–2.9 eggs/week, 0.91 (0.84–0.99) for those consuming 3.0–5.9 eggs/week, and 0.95 (0.86–1.04) for those consuming ≥ 6.0 eggs/week.

Few studies have been conducted to investigate the association between egg consumption and dementia. In Italy, Nicoli et al. [30] examined data from 1390 participants aged ≥ 80 years from a cross-sectional study in the Varese province and found that the adjusted OR of dementia in the middle tertile of egg consumption compared to the lowest tertile was 0.60 (0.47–0.77), while the OR in the highest tertile of egg consumption was 0.63 (0.38–1.04). The authors further analysed data from 512 participants in the cohort follow-up and found that the corresponding HRs were 0.68 (0.39–1.17) and 0.85 (0.64–1.14), suggesting no significant association. In Finland, Ylilauri et al. [21] carried out a cohort study of 2497 men aged 42–60 y, followed up for 21.9 years, and observed that each additional 0.5 eggs (27 g)/d was associated with a hazard ratio (HR) of 0.89 (95% CI 0.78–1.01) but not significantly. In Spain, Margara-Escudero et al. [31] anlaysed data from 25,015 participants aged 30–70 years from the European Prospective Investigation into Cancer and Nutrition (EPIC)-Spain Dementia Cohort. Cohort participants were recruited between 1992 and 1996 for the baseline survey and followed up for a mean of 21.5 years. The authors found no association between egg consumption and dementia; the adjusted HR for the 4th quartile vs. the 1st quartile of egg consumption was 1.05 (0.85–1.31). After dividing the population by adherence to the relative Mediterranean diet (rMED) score, they observed an inverse association between egg consumption and dementia in participants with low adherence to the rMED score (HR in Q4 vs. Q1: 0.52, 95% CI 0.30–0.90). But there was no association between participants having medium adherence (1.20, 0.89–1.62) and high adherence to the rMED score (0.93, 0.61–1.39). Our study in China revealed a significant and inverse association between egg consumption and dementia among participants who consumed eggs Monthly, Weekly and Daily. In other words, our study demonstrated that the risk of dementia was significantly reduced in these adults who consumed eggs Daily. This protective effect of Daily consumption was consistently observed regardless of whether Monthly or Weekly consumption was taken for comparison (Table 5).

Our study found that participants who consumed eggs at a frequency of ≥Twice a day might have an increased OR of dementia compared to those who consumed eggs at a frequency of Non-consuming/<monthly (Table 5) or participants who consumed eggs Daily (Table 4), approaching statistical significance. The finding suggests a possible link between excessive egg consumption and dementia risk, likely due to the high cholesterol content of eggs, with each egg containing ~200 mg of cholesterol. Previous studies using randomized controlled trials (RCTs) data [12] have revealed that individuals who consumed more than four whole eggs per week experienced greater elevations in blood total cholesterol, HDL cholesterol and LDL cholesterol compared to those who consumed equivalent amounts of egg substitutes. Animal studies involving mice, rats and rabbits have demonstrated an association between high cholesterol intake and AD-type pathologies [32,33,34]. Some human studies have also shown an association between dietary cholesterol intake and lower cognitive performance [35,36]. Furthermore, recent population-based cohort research found a positive association between blood cholesterol levels and incident dementia [37]. Our study observed an increased OR of dementia with the consumption of eggs ≥Twice a day, but it did not reach conventional statistical significance, which was probably due to the small number of participants in this category of egg consumption. Nonetheless, the potential impact of excessive egg consumption on dementia warrants further investigation.

Our study did not find a significant increase in the OR of dementia among participants who reported non-consuming/<monthly over the past two years. There is no research examining this low level of egg consumption in relation to dementia [30]. However, previous research examining cognitive impairment in China found a relation to non-consumers or <weekly consumers; the risk of CI was significantly increased in comparison to those consuming 0.1–2.9 eggs/week or 3.0–5.9 eggs/week [29]. Also, such a group of never/rarely consuming eggs was found to have an increased risk of CVD, particularly among older people [28]. In China, eggs are a popular food due to their nutritional value, affordability and ease of preparation [22]. Despite this, our study found that 13.5% of older adults did not eat eggs or consumed them less than monthly during the two-year period. The reasons for this low consumption could be attributed to poverty. Our data showed that participants with lower family income had reduced egg consumption. These individuals who did not eat eggs over the past two years also had decreased consumption of other nutrient-rich foods such as meats, fish, vegetables and fruits (Table 2). It is worth noting that they may represent a specific subset of the older population, warranting further investigation.

Our study demonstrated that participants who consumed eggs Daily had a reduced odds ratio of dementia compared to those who consumed eggs Monthly or Weekly, regardless of the confounders adjusted for in the analysis. The protective effect of Daily egg consumption against dementia in older adults may be attributed to the presence of bioactive compounds and numerous other nutrients such as high-quality protein, unsaturated fatty acids and vitamins [38]. The nutrient-dense nature of eggs makes them a valuable source of energy, particularly for individuals at risk of malnutrition, such as older adults [39]. Previous research from RCT data [12] indicated that compared to individuals consuming ≤ 4 whole eggs per week, those consuming > 4 whole eggs per week did not experience elevated blood pressure, lipids and lipoproteins. This suggests that the increased egg consumption in our study would not be likely to contribute to cardiovascular risk, which thereby increases the incidence of dementia. Bioactive compounds like lutein, zeaxanthin and choline found in eggs may have beneficial effects on intestinal cholesterol absorption. On the other hand, due to the high levels of protein in eggs, increased egg consumption may delay sarcopenia in older adults [40], while sarcopenia could be associated with an increased risk of dementia [41].

Available evidence indicates that brain inflammation is frequently present in the pathology of dementia. This inflammation, caused by misfolded proteins, such as tau proteins, amyloid beta and alpha-synuclein, could activate microglia toll-like receptors (TLRs) and trigger an innate immune response, which in turn produces inflammatory mediators [42]. Furthermore, neuroinflammation harms the blood–brain barrier’s integrity, increasing the risk of dementia. Consumption of foods such as eggs, which contain antioxidants, choline and omega-3 fatty acids, has been linked to a decrease in systemic inflammation [43,44]. The bioactive components in eggs have anti-inflammatory qualities and may, therefore, contribute to the prevention of dementia [9,45]. Consumption of eggs has also been found to lower the risk of cardiovascular disease in Asian populations [28,46]. Qin et al. [28] examined data from a cohort study of half a million participants in China and revealed that daily egg consumption, compared to non-consuming, was associated with a lower risk of CVD (HR 0.89, 0.87–0.92) [28]. Egg’s components, including antioxidants and anti-inflammatory qualities, as well as their potential to lower the CVD risk, could help reduce the risk of dementia. Previous studies [3,47,48] have also found that the consumption of fish, vegetables and fruits can reduce the risk of dementia since these dietary intakes contain antioxidants and omega-3 fatty acids. The data of our study showed that there were positive associations between these dietary intakes and egg consumption (Table 2). The finding that daily egg consumption reduces dementia risk in our study is in line with the results of previous studies examining the impact of fish, vegetables and fruits consumption on dementia [3,47,48].

Our study examining data from this population-based case-control study in China identified that eating one egg per day could reduce the risk of dementia. The study findings contribute to the development of better policies and improve public health aimed at reducing the burden of disease by promoting egg consumption among older adults.

Strengths and Limitations of This Study

To the best of our knowledge, this study is the first to examine the association between egg consumption and dementia in China, a country with the largest number of people with dementia and the highest egg consumption worldwide. It is also the first to report a significant association between daily egg consumption and a reduced risk of all types of dementia in the world. Our study produces new insights suggesting that daily egg consumption may be associated with a reduced risk of dementia. We included important confounders for adjustment, such as educational level, smoking, alcohol consumption, CVD, depression and consumption of red meats, fish, vegetables and fruits apart from age, thereby minimising residual effects. Additionally, we performed sensitivity analyses using different levels of egg consumption as references, ensuring the robustness of our findings. This study has limitations. First, there were significant age differences between the case and control groups due to the lack of individual age matching in the case-control design for data collection. However, in the data analysis, we adjusted for age as a continuous variable, thereby minimising the residual effect of age on the association between egg consumption and dementia risk. Furthermore, we performed separate data analysis by age of <75 years (mean age was 62.3 in people with dementia vs. 65.1 in people without dementia) and ≥75 years (81.8 vs. 75.3) and found that the results were similar to those from the overall data analysis; for example, the data from Monthly, Weekly to Daily egg consumption showed a significantly reduced odds of dementia per average increment in egg consumption from Monthly, Weekly to Daily in the age group of <75 years (Model 3-adjusted OR 0.22, 0.08–0.61) and in the age group of ≥75 years (0.45, 0.22–0.93). Second, our food frequency questionnaire collected data on the frequency of egg consumption but did not measure the quantity of eggs consumed at each level of the frequency. It may have diluted the association we identified. Previous research suggests that the daily consumption of eggs among Chinese adults usually amounts to 0.76 egg/day [28]. We analysed the frequencies of egg consumption to determine the association between egg intake and dementia and found that Daily egg consumption was associated with a lower risk of dementia in Chinese adults. Third, the case-control design of our study limits the ability to refer causality inference in the association between egg consumption and dementia. However, the observed association between increased egg consumption from Monthly to Daily and reduced risk of dementia is consistent with findings from a recently published study in Western populations [49]. Pan et al. examined data from 1024 older Americans with a mean age of 81.4 who were followed up for 6.7 years in the Rush Memory and Aging Project cohort and found that the risk of Alzheimer’s dementia was significantly reduced with Weekly consumption of >1 egg/wk (adjusted hazard ratio 0.53, 95% CI 0.34–0.83) and ≥2 eggs/wk (0.53, 0.35–0.81), compared to those who consumed ≤1 egg/wk [49]. The trend for the protective effect of egg consumption on dementia is consistent with the findings of our study. Nevertheless, cohort studies in China are required to further examine the protective effect of Daily egg consumption on dementia.

Consult your Doctor

कमी फायबर आहार हा उच्च-जोखीम कोरोनरी प्लेकसंबंधित आहे.

 संदर्भ

कार्डिओव्हस्क रेस. २०२५ जून १६; १२१(८): १२०४–१२१४. doi: 10.1093/cvr/cvaf088

 कमी फायबर आहार हा उच्च-जोखीम कोरोनरी प्लेक वैशिष्ट्यांशी संबंधित आहे इंग्रिड लार्सन 1,2, जियांगमिंग सन 3, शफकत अहमद 4,5,6, गोरन बर्गस्ट्रोम 7,8, कार्ल-जोहान कार्लहॉल 9,10,11, 

केर्स्टिन सेडरलंड 12, इसाबेल ड्रेक 13, जॅन एंगवाल 14,15, एरिक्सन 15,17, 16,17 हॅगस्ट्रोम 18, टॉमस जेर्नबर्ग 19, तंजा केरो 20,21, क्रिस्टर लिंडमार्क 22,23, मारिया मॅनिला 24, मार्जू ओरहो-मेलँडर 25, अराज रावशानी 26,27, उल्फ रिसेरस 28, ॲनिका रोसेन्ग्रेन 29,30, मॅट्स रायबर्ग ३१, कॅरोलिन श्मिट ३२, एमिली सोनेस्टेड ३३, मारिया वेनबर्ग ३४, कार्ल योहान ओस्टग्रेन ३५,३६, इसाबेल गोन्काल्वेस ३७,३८,२,✉,३

प्रस्तावना

आहार हा आजाराचा एक महत्त्वाचा निर्धारक आहे.१

मेडिटेरेनियन आहार आणि तत्सम पद्धती२

हृदय व रक्तवाहिन्यांसंबंधी आजार३ आणि मृत्यूचा कमी धोका यांच्याशी संबंधित असल्याचे आढळले आहे.२,४,५

विविध आहार निर्देशांकांनी मेडिटेरेनियन आणि इतर उच्च-तंतुमय आहारांसारख्या पद्धती ओळखल्या आहेत, ज्या आजाराचा कमी धोका यांच्याशी संबंधित

 असण्याची शक्यता आहे.५

हृदय व रक्तवाहिन्यांसंबंधी आजार (CVD) हे मृत्यू आणि अपंगत्वाचे 

सर्वात महत्त्वाचे कारण आहे,६

ज्यात कोरोनरी रोग हे अकाली मृत्यूचे प्रमुख कारण आहे.

सर्वात सामान्य मूळ कारण एथेरोस्क्लेरोसिस आहे, जिथे अनेक दशकांपासून प्लाक तयार होतात, त्यापैकी काही फुटण्याची शक्यता असते,७

ज्यामुळे मायोकार्डियल इन्फार्क्शन, किंवा अचानक कोरोनरी मृत्यू होतो. तथापि, कोरोनरी घटनांचा संबंध केवळ प्लाकमुळे होणाऱ्या स्टेनोसिसच्या प्रमाणाशीच नाही,

तर प्लाकच्या रचनेशीही आहे.8

तरीही, फुटण्याची शक्यता असलेले प्लाक शोधण्यासाठी सहज उपलब्ध असलेल्या नॉन-इन्व्हेसिव्ह निदान पद्धतींचा अभाव होता. अलिकडच्या वर्षांत, कोरोनरी कम्प्युटेड टोमोग्राफी अँजिओग्राफी (CCTA) एक आशादायक पद्धत म्हणून उदयास आली आहे आणि कमी/मध्यम जोखमीच्या रुग्णांच्या जोखीम वर्गीकरणासाठी आंतरराष्ट्रीय मार्गदर्शक तत्त्वांमध्ये तिची शिफारस केली जाते.९,१०

प्रतिकूल किंवा उच्च-जोखीम वैशिष्ट्ये असलेले प्लेक्स, उदाहरणार्थ लक्षणीय स्टेनोसिससह CCTA वरील कमी अॅटेन्युएशन, हे हृदय व रक्तवाहिन्यांसंबंधी घटनांच्या उच्च जोखमीशी जोडले गेले आहेत.११,१२

ज्या आहार पद्धतींमध्ये भाज्या, फळे आणि संपूर्ण धान्यांचा जास्त समावेश असतो, त्या हृदय व रक्तवाहिन्यांसंबंधी रोगांच्या (CVD) कमी जोखमीशी संबंधित आहेत.१,३,१३

आहार निर्देशांक हे अशा खाद्यपदार्थांपासून तयार केलेले संयुक्त चल म्हणून वापरले गेले आहेत, जे आधीच आरोग्यदायी किंवा अनारोग्यदायी म्हणून ओळखले जातात.५,१३

कालुझा आणि सहकाऱ्यांनी१४ एका फूड फ्रिक्वेन्सी प्रश्नावलीमधून (FFQ) असे खाद्यपदार्थ ओळखले, जे उच्च संवेदनशीलता सी-रिॲक्टिव्ह प्रोटीनच्या (hsCRP) वाढलेल्या पातळीसारख्या दाह निर्देशांकांशी संबंधित होते आणि त्यांनी दाह-विरोधी क्षमता असलेल्या पदार्थांचा (फळे आणि भाज्या, सुकामेवा, संपूर्ण धान्य) समावेश असलेल्या आहार निर्देशांकामध्ये (DI) त्यांचे गट केले. ब्रेड, ब्रेकफास्ट सिरियल्स आणि ओटमील, कमी फॅट असलेले चीज, कॅनोला आणि ऑलिव्ह तेल, कॉफी, चहा, चॉकलेट, रेड वाईन आणि बिअर) आणि दाह निर्माण करण्याची क्षमता असलेले पदार्थ (प्रक्रिया न केलेले आणि प्रक्रिया केलेले लाल मांस, अवयव, बटाटा चिप्स आणि साखरयुक्त पेये).¹⁴ स्वीडिश प्रॉस्पेक्टिव्ह कोहोर्ट अभ्यासांमध्ये, उच्च डीआय (DI) आणि दाह निर्माण करण्याची क्षमता असलेल्या पदार्थांचे कमी सेवन करणाऱ्या पुरुष आणि महिलांमध्ये, कमी डीआय (DI) असलेल्यांच्या तुलनेत, १६ वर्षांच्या फॉलो-अप नंतर मृत्यूचा धोका कमी होता,¹⁵

पोटातील महाधमनीचा ॲन्युरिझम,¹⁶

आणि हृदय निकामी होण्याचा धोका¹⁷. आयसोटोप-रेशो मास स्पेक्ट्रोमेट्रीचा वापर करून, हे सिद्ध झाले आहे की आहारातील सेवन हे फुटण्याची शक्यता असलेल्या प्लाकच्या घटकांमध्ये प्रतिबिंबित होते.¹⁸

तथापि, मोठ्या लोकसंख्या-आधारित कोहोर्ट्समध्ये आहारातील सेवन आणि सीसीटीए (CCTA) मधील कोरोनरी धमनी प्लाकची उपस्थिती किंवा त्यांची वैशिष्ट्ये यांच्यातील संभाव्य संबंध अद्याप अज्ञात आहेत.

या अभ्यासाचा उद्देश, कालुझा एट अल.¹⁴ यांच्या दाह-विरोधी आहार निर्देशांकावर (anti-inflammatory DI) आधारित आहार निर्देशांकाद्वारे मूल्यांकन केलेले आहार सेवन, हे यादृच्छिकपणे निवडलेल्या, मध्यमवयीन स्वीडिश व्यक्तींच्या लोकसंख्या-आधारित गटात कोरोनरी एथेरोस्क्लेरोसिस, CCTA द्वारे मूल्यांकन केलेली कोरोनरी प्लाकची वैशिष्ट्ये आणि ज्ञात हृदय व रक्तवाहिन्यांसंबंधी जोखीम घटकांशी संबंधित आहे की नाही याचे विश्लेषण करणे हा होता.

गृहीतक असे होते की, आहारात तंतुमय पदार्थांचे (फायबर) प्रमाण कमी असणे आणि लाल व प्रक्रिया केलेल्या मांसाचे सेवन जास्त असणे, हे अधिक प्रतिकूल किंवा उच्च-जोखीम असलेल्या कोरोनरी प्लाकच्या वैशिष्ट्यांशी संबंधित होते.