1:07 muscle mass in Sout Asians [1], [2] 1:14 sarcopenia[3], [4] 1:34 brown fat?[5], [6], [7] 2:07 brown fat in infants[8] 2:31 brown fat reduces inflammation [9] 2:37 increased brown fat mass in the insulin sensitive[10] 2:42 reduced brown fat in insulin resistance[10] 2:47 anatomical locations of brown fat[11] 2:59 PET scan and MRI to image brown fat[12], [13] 3:05 infrared / thermal imaging for brown fat[14], [15] 3:38 uncoupling protein-1 (UCP-1) and brown fat[16], [17], [18] 4:00 failure to activate brown fat in south Asian upon cold exposure[19], [20] 4:19 Nutraceuticals and UCP-1 activation[21] 4:40 Rice consumption upon Latin Americans[22] 4:54 metabolic diseases among Hispanics[23], [24] 5:05 obesogenic environment[25] 5:15 pollutants and obesity[21] 7:15 Arsenic in rice[26], [27] 7:20 Arsenic & obesity and metabolic syndrome[28], [29], [30] 7:29 Arsenic deactivated brown fat[29], [31] 8:05 temperature and climate to activate brown fat [32] 10:08 diabetes reversal talk by Malaysia Kini - search for “Reverse Obesity and Type 2 Diabetes with Roczen Malaysiakini” 11:45 Gut microbiota and appendicitis[33] 12:00 lean / thin people have higher brown fat[11] 12:15 brown fat is inversely proportional to visceral fat[34], [35] 12:25 UCP-1 could be switched on[36], [37], [38] 13:10 Aborigines in New Zealand and heart attack genes, calcification [39], [40], [41] 13:28 Nattokinase, fermented food consumption [42] 13:48 Vitamin D3 absorption is better when vitamin K2 and K7 is adequate[43], [44] 13:58 Gut microbiome and ischemic heart diseases[45], [46] 18:14 Rebound with GLP-1[47], [48] 18:28 GLP-1 is a secretin[49] 18:35 Hyperinsulinemic states and mortality[50] 22:06 palm oil boiling point and aldehyde production[51], [52] 22:18 Virgin olive oil cooking and aldehyde production[53], [54] 22:30 seed / vegetable oils and aldehyde production[53], [54] 23:30 Vit A,E, CoQ10 in red palm oil is underutilized in preventive cardiology[55], [56] 28:33 Insulin resistance, sensitivity calculation. HOMA-IR, HOMA-2B[57] 28:48 Triglyceride-Glucose index[58] 29:02 UTM Diabetes subcluster preprint - “Subclustering of Type 2 Diabetes for Better Personalisation Treatment Management Using K-Means Clustering Algorithm” 29:26 Precision diabetes management according to subclusters[59], [60] 31:34 China 7 diabetes clusters and 5 clusters in Japan [61], [62] 31:52 Type 1.5 Diabetes, LADA, Autoimmune diabetes[63] 32:20 Fructose toxicity in diabetes[64], [65] 32:46 exogenous, injectable insulin cost and healthcare burden[66], [67], [68], [69] 32:55 SLGT 2 inhibitors and cardioprotection[70] 33:34 Resistant starch type 3 on starch / rice [66] 33:48 Resistant starch type 5: Lipid-Amylose complex [71]
Though Dr Bhuwan is very knowledgeable and his intentions are very very good, i find this podcast is abit all over the place and hard to follow. But i guess some people need these kinds of podcasts. For me its simple, no processed food, LOW sugar, eat in moderation. This is simple & fit for all. Talking about genetics and all that makes it so complicated more than it is. Why atuk nenek eat so much rice yet not so much problem.. SUGAR, PROCESSED FOOD.
[1] A. Misra et al., “Body fat, metabolic syndrome and hyperglycemia in South Asians,” J Diabetes Complications, vol. 32, no. 11, pp. 1068-1075, Nov. 2018, doi: 10.1016/j.jdiacomp.2018.08.001. [2] E. Pomeroy, V. Mushrif-Tripathy, T. J. Cole, J. C. K. Wells, and J. T. Stock, “Ancient origins of low lean mass among South Asians and implications for modern type 2 diabetes susceptibility,” Sci Rep, vol. 9, no. 1, p. 10515, Jul. 2019, doi: 10.1038/s41598-019-46960-9. [3] C. Salom Vendrell, E. García Tercero, J. B. Moro Hernández, and B. A. Cedeno-Veloz, “Sarcopenia as a Little-Recognized Comorbidity of Type II Diabetes Mellitus: A Review of the Diagnosis and Treatment,” Nutrients, vol. 15, no. 19, p. 4149, Sep. 2023, doi: 10.3390/nu15194149. [4] H. Chen, X. Huang, M. Dong, S. Wen, L. Zhou, and X. Yuan, “The Association Between Sarcopenia and Diabetes: From Pathophysiology Mechanism to Therapeutic Strategy,” Diabetes, Metabolic Syndrome and Obesity, vol. Volume 16, pp. 1541-1554, May 2023, doi: 10.2147/DMSO.S410834. [5] S. Cinti, “Pink Adipocytes,” Trends in Endocrinology & Metabolism, vol. 29, no. 9, pp. 651-666, Sep. 2018, doi: 10.1016/j.tem.2018.05.007. [6] S. Enerbäck, “Human Brown Adipose Tissue,” Cell Metab, vol. 11, no. 4, pp. 248-252, Apr. 2010, doi: 10.1016/j.cmet.2010.03.008. [7] A. S. Karanfil, F. Louis, and M. Matsusaki, “Biofabrication of vascularized adipose tissues and their biomedical applications,” Mater Horiz, vol. 10, no. 5, pp. 1539-1558, 2023, doi: 10.1039/D2MH01391F. [8] M. E. Lidell, “Brown Adipose Tissue in Human Infants,” 2018, pp. 107-123. doi: 10.1007/164_2018_118. [9] M. C. Soler-Vázquez, P. Mera, S. Zagmutt, D. Serra, and L. Herrero, “New approaches targeting brown adipose tissue transplantation as a therapy in obesity,” Biochem Pharmacol, vol. 155, pp. 346-355, Sep. 2018, doi: 10.1016/j.bcp.2018.07.022. [10] K. Maliszewska and A. Kretowski, “Brown Adipose Tissue and Its Role in Insulin and Glucose Homeostasis,” Int J Mol Sci, vol. 22, no. 4, p. 1530, Feb. 2021, doi: 10.3390/ijms22041530. [11] B. P. Leitner et al., “Mapping of human brown adipose tissue in lean and obese young men,” Proceedings of the National Academy of Sciences, vol. 114, no. 32, pp. 8649-8654, Aug. 2017, doi: 10.1073/pnas.1705287114. [12] K. Maliszewska, E. Adamska-Patruno, K. Miniewska, W. Bauer, M. Mojsak, and A. Kretowski, “PET/MRI-evaluated brown adipose tissue activity may be related to dietary MUFA and omega-6 fatty acids intake,” Sci Rep, vol. 12, no. 1, p. 4112, Mar. 2022, doi: 10.1038/s41598-022-08125-z. [13] M. Wu, D. Junker, R. T. Branca, and D. C. Karampinos, “Magnetic Resonance Imaging Techniques for Brown Adipose Tissue Detection,” Front Endocrinol (Lausanne), vol. 11, Aug. 2020, doi: 10.3389/fendo.2020.00421. [14] Q. Y. Ang et al., “A new method of infrared thermography for quantification of brown adipose tissue activation in healthy adults (TACTICAL): a randomized trial,” The Journal of Physiological Sciences, vol. 67, no. 3, pp. 395-406, May 2017, doi: 10.1007/s12576-016-0472-1. [15] J. Law, D. E. Morris, H. Budge, and M. E. Symonds, “Infrared Thermography,” 2018, pp. 259-282. doi: 10.1007/164_2018_137. [16] R. Huang et al., “Ethnicity Differences in the Association of UCP1-3826A/G, UCP2-866G/A and Ala55Val, and UCP3-55C/T Polymorphisms with Type 2 Diabetes Mellitus Susceptibility: An Updated Meta-Analysis,” Biomed Res Int, vol. 2021, pp. 1-14, Oct. 2021, doi: 10.1155/2021/3482879. [17] K.-H. Lee, V.-Y. Chai, S. S. Kanachamy, and Y.-H. Say, “Association of UCP1 -3826A/G and UCP3 -55C/T gene polymorphisms with obesity and its related traits among multi-ethnic Malaysians.,” Ethn Dis, vol. 25, no. 1, pp. 65-71, 2015. [18] L. de A. Brondani, T. S. Assmann, G. C. K. Duarte, J. L. Gross, L. H. Canani, and D. Crispim, “The role of the uncoupling protein 1 (UCP1) on the development of obesity and type 2 diabetes mellitus,” Arquivos Brasileiros de Endocrinologia & Metabologia, vol. 56, no. 4, pp. 215-225, Jun. 2012, doi: 10.1590/S0004-27302012000400001. [19] M. E. Symonds, “Ethnicity and its effects on brown adipose tissue,” Lancet Diabetes Endocrinol, vol. 2, no. 3, pp. 185-186, Mar. 2014, doi: 10.1016/S2213-8587(13)70177-3. [20] L. E. H. Bakker et al., “Brown adipose tissue volume in healthy lean south Asian adults compared with white Caucasians: a prospective, case-controlled observational study,” Lancet Diabetes Endocrinol, vol. 2, no. 3, pp. 210-217, Mar. 2014, doi: 10.1016/S2213-8587(13)70156-6. [21] A. Armani, A. Feraco, E. Camajani, S. Gorini, M. Lombardo, and M. Caprio, “Nutraceuticals in Brown Adipose Tissue Activation,” Cells, vol. 11, no. 24, p. 3996, Dec. 2022, doi: 10.3390/cells11243996. [22] S. P. Batres-Marquez, H. H. Jensen, and J. Upton, “Rice Consumption in the United States: Recent Evidence from Food Consumption Surveys,” J Am Diet Assoc, vol. 109, no. 10, pp. 1719-1727, Oct. 2009, doi: 10.1016/j.jada.2009.07.010. [23] T. M. Paixão et al., “Systematic Review and Meta-Analysis of Metabolic Syndrome and Its Components in Latino Immigrants to the USA,” Int J Environ Res Public Health, vol. 20, no. 2, p. 1307, Jan. 2023, doi: 10.3390/ijerph20021307. [24] G. Heiss et al., “Prevalence of Metabolic Syndrome Among Hispanics/Latinos of Diverse Background: The Hispanic Community Health Study/Study of Latinos,” Diabetes Care, vol. 37, no. 8, pp. 2391-2399, Aug. 2014, doi: 10.2337/dc13-2505. [25] N. Perakakis, O. M. Farr, and C. S. Mantzoros, “Leptin in Leanness and Obesity,” J Am Coll Cardiol, vol. 77, no. 6, pp. 745-760, Feb. 2021, doi: 10.1016/j.jacc.2020.11.069. [26] M. R. Karagas et al., “Rice Intake and Emerging Concerns on Arsenic in Rice: a Review of the Human Evidence and Methodologic Challenges,” Curr Environ Health Rep, vol. 6, no. 4, pp. 361-372, Dec. 2019, doi: 10.1007/s40572-019-00249-1. [27] L. J. Su, T.-C. Chiang, and S. N. O’Connor, “Arsenic in brown rice: do the benefits outweigh the risks?,” Front Nutr, vol. 10, Jul. 2023, doi: 10.3389/fnut.2023.1209574. [28] B. L. Sánchez-Rodríguez, I. Castillo-Maldonado, D. Pedroza-Escobar, D. Delgadillo-Guzmán, and M. F. Soto-Jiménez, “Association of obesity, diabetes, and hypertension with arsenic in drinking water in the Comarca Lagunera province (north-central Mexico),” Sci Rep, vol. 13, no. 1, p. 9244, Jun. 2023, doi: 10.1038/s41598-023-36166-5. [29] S.-H. Ro et al., “Arsenic Toxicity on Metabolism and Autophagy in Adipose and Muscle Tissues,” Antioxidants, vol. 11, no. 4, p. 689, Mar. 2022, doi: 10.3390/antiox11040689. [30] P. Pánico et al., “Is Arsenic Exposure a Risk Factor for Metabolic Syndrome? A Review of the Potential Mechanisms,” Front Endocrinol (Lausanne), vol. 13, May 2022, doi: 10.3389/fendo.2022.878280. [31] S. Ro, Y. Jang, and J. Bae, “Brown adipose tissue metabolism in arsenic environmental health and obesity,” The FASEB Journal, vol. 33, no. S1, Apr. 2019, doi: 10.1096/fasebj.2019.33.1_supplement.lb271. [32] P. Lee et al., “Temperature-Acclimated Brown Adipose Tissue Modulates Insulin Sensitivity in Humans,” Diabetes, vol. 63, no. 11, pp. 3686-3698, Nov. 2014, doi: 10.2337/db14-0513. [33] Z. Wang et al., “Causal effects of gut microbiota on appendicitis: a two-sample Mendelian randomization study,” Front Cell Infect Microbiol, vol. 13, Dec. 2023, doi: 10.3389/fcimb.2023.1320992. [34] S. E. Da Rosa, E. B. Neves, E. C. Martinez, R. A. Marson, and V. M. Reis, “Subcutaneous and Visceral Fat: Relation with Brown Adipose Tissue Activation in Women,” Sports Med Int Open, vol. 08, no. CP, Jan. 2024, doi: 10.1055/a-2187-6974. [35] A. G. Wibmer et al., “Brown adipose tissue is associated with healthier body fat distribution and metabolic benefits independent of regional adiposity,” Cell Rep Med, vol. 2, no. 7, p. 100332, Jul. 2021, doi: 10.1016/j.xcrm.2021.100332. [36] K. Onodera et al., “A newly identified compound activating UCP1 inhibits obesity and its related metabolic disorders,” Obesity, vol. 32, no. 2, pp. 324-338, Feb. 2024, doi: 10.1002/oby.23948
[37] U. Jagtap and A. Paul, “UCP1 activation: Hottest target in the thermogenesis pathway to treat obesity using molecules of synthetic and natural origin,” Drug Discov Today, vol. 28, no. 9, p. 103717, Sep. 2023, doi: 10.1016/j.drudis.2023.103717. [38] I. Hachemi and M. U-Din, “Brown Adipose Tissue: Activation and Metabolism in Humans,” Endocrinology and Metabolism, vol. 38, no. 2, pp. 214-222, Apr. 2023, doi: 10.3803/EnM.2023.1659. [39] D. L. Duffy et al., “Familial aggregation of albuminuria and arterial hypertension in an Aboriginal Australian community and the contribution of variants in ACE and TP53,” BMC Nephrol, vol. 17, no. 1, p. 183, Dec. 2016, doi: 10.1186/s12882-016-0396-2. [40] S. Nath, B. Poirier, X. Ju, K. Kapellas, D. Haag, and L. Jamieson, “Periodontal disease inequities among Indigenous populations: A systematic review and meta‐analysis,” J Periodontal Res, vol. 57, no. 1, pp. 11-29, Feb. 2022, doi: 10.1111/jre.12942. [41] G. Mudd-Martin et al., “Considerations for Cardiovascular Genetic and Genomic Research With Marginalized Racial and Ethnic Groups and Indigenous Peoples: A Scientific Statement From the American Heart Association,” Circ Genom Precis Med, vol. 14, no. 4, Aug. 2021, doi: 10.1161/HCG.0000000000000084. [42] H. Chen et al., “Nattokinase: A Promising Alternative in Prevention and Treatment of Cardiovascular Diseases,” Biomark Insights, vol. 13, p. 117727191878513, Jan. 2018, doi: 10.1177/1177271918785130. [43] A. J. van Ballegooijen, S. Pilz, A. Tomaschitz, M. R. Grübler, and N. Verheyen, “The Synergistic Interplay between Vitamins D and K for Bone and Cardiovascular Health: A Narrative Review,” Int J Endocrinol, vol. 2017, pp. 1-12, 2017, doi: 10.1155/2017/7454376. [44] N. Jadhav et al., “Molecular Pathways and Roles for Vitamin K2-7 as a Health-Beneficial Nutraceutical: Challenges and Opportunities,” Front Pharmacol, vol. 13, Jun. 2022, doi: 10.3389/fphar.2022.896920. [45] A. Nesci et al., “Gut Microbiota and Cardiovascular Disease: Evidence on the Metabolic and Inflammatory Background of a Complex Relationship,” Int J Mol Sci, vol. 24, no. 10, p. 9087, May 2023, doi: 10.3390/ijms24109087. [46] A. Al Samarraie, M. Pichette, and G. Rousseau, “Role of the Gut Microbiome in the Development of Atherosclerotic Cardiovascular Disease,” Int J Mol Sci, vol. 24, no. 6, p. 5420, Mar. 2023, doi: 10.3390/ijms24065420. [47] J. P. H. Wilding et al., “Weight regain and cardiometabolic effects after withdrawal of semaglutide: The STEP 1 trial extension,” Diabetes Obes Metab, vol. 24, no. 8, pp. 1553-1564, Aug. 2022, doi: 10.1111/dom.14725. [48] R. Caro, D. Samsel, and P. Savel, “Is there sustained weight loss after discontinuation of GLP-1 agonist for obesity treatment?,” Evidence-Based Practice, vol. 26, no. 5, pp. 7-8, May 2023, doi: 10.1097/EBP.0000000000001786. [49] A. R. Meloni, M. B. DeYoung, C. Lowe, and D. G. Parkes, “GLP‐1 receptor activated insulin secretion from pancreatic β‐cells: mechanism and glucose dependence,” Diabetes Obes Metab, vol. 15, no. 1, pp. 15-27, Jan. 2013, doi: 10.1111/j.1463-1326.2012.01663.x. [50] X. Shen et al., “Phenotype of higher post-load insulin response as a predictor of all-cause mortality and cardiovascular mortality in the Chinese non-diabetic population,” Diabetol Metab Syndr, vol. 14, no. 1, Dec. 2022, doi: 10.1186/s13098-022-00786-0. [51] A. A.-W. Japir, J. Salimon, D. Derawi, M. Bahadi, and M. R. Yusop, “Separation of free fatty acids from high free fatty acid crude palm oil using short-path distillation,” 2016, p. 030001. doi: 10.1063/1.4966739. [52] K. G. Berger, “PALM OIL,” in Encyclopedia of Food Sciences and Nutrition, Elsevier, 2003, pp. 4325-4331. doi: 10.1016/B0-12-227055-X/01348-1. [53] C.-Y. Peng, C.-H. Lan, P.-C. Lin, and Y.-C. Kuo, “Effects of cooking method, cooking oil, and food type on aldehyde emissions in cooking oil fumes,” J Hazard Mater, vol. 324, pp. 160-167, Feb. 2017, doi: 10.1016/j.jhazmat.2016.10.045. [54] S. Moumtaz, B. C. Percival, D. Parmar, K. L. Grootveld, P. Jansson, and M. Grootveld, “Toxic aldehyde generation in and food uptake from culinary oils during frying practices: peroxidative resistance of a monounsaturate-rich algae oil,” Sci Rep, vol. 9, no. 1, p. 4125, Mar. 2019, doi: 10.1038/s41598-019-39767-1. [55] R. Loganathan, K. M. Subramaniam, A. K. Radhakrishnan, Y.-M. Choo, and K.-T. Teng, “Health-promoting effects of red palm oil: evidence from animal and human studies,” Nutr Rev, vol. 75, no. 2, pp. 98-113, Feb. 2017, doi: 10.1093/nutrit/nuw054. [56] C. H. Tan, C. J. Lee, S. N. Tan, D. T. S. Poon, C. Y. E. Chong, and L. P. 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Shimabukuro, “Novel strategies for glycaemic control and preventing diabetic complications applying the clustering-based classification of adult-onset diabetes mellitus: A perspective,” Diabetes Research and Clinical Practice, vol. 180. Elsevier Ireland Ltd, Oct. 01, 2021. doi: 10.1016/j.diabres.2021.109067. [61] X. Xiong, Y. Yang, L. Wei, Y. Xiao, L. Li, and L. Sun, “Identification of two novel subgroups in patients with diabetes mellitus and their association with clinical outcomes: A two‐step cluster analysis,” J Diabetes Investig, vol. 12, no. 8, pp. 1346-1358, Aug. 2021, doi: 10.1111/jdi.13494. [62] H. Tanabe et al., “Factors Associated with Risk of Diabetic Complications in Novel Cluster-Based Diabetes Subgroups: A Japanese Retrospective Cohort Study,” J Clin Med, vol. 9, no. 7, p. 2083, Jul. 2020, doi: 10.3390/jcm9072083. [63] S. Pieralice and P. Pozzilli, “Latent Autoimmune Diabetes in Adults: A Review on Clinical Implications and Management,” Diabetes Metab J, vol. 42, no. 6, p. 451, 2018, doi: 10.4093/dmj.2018.0190. [64] J. P. Bantle, “Dietary Fructose and Metabolic Syndrome and Diabetes,” J Nutr, vol. 139, no. 6, pp. 1263S-1268S, Jun. 2009, doi: 10.3945/jn.108.098020. [65] Y. Kawano and D. E. Cohen, “Mechanisms of hepatic triglyceride accumulation in non-alcoholic fatty liver disease,” J Gastroenterol, vol. 48, no. 4, pp. 434-441, Apr. 2013, doi: 10.1007/s00535-013-0758-5. [66] C. E. Klostermann, P. L. Buwalda, H. Leemhuis, P. de Vos, H. A. Schols, and J. H. Bitter, “Digestibility of resistant starch type 3 is affected by crystal type, molecular weight and molecular weight distribution,” Carbohydr Polym, vol. 265, p. 118069, Aug. 2021, doi: 10.1016/j.carbpol.2021.118069. [67] K. 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Emmambux, “Amylose-lipid complex production and potential health benefits: A mini‐review,” Starch - Stärke, vol. 69, no. 7-8, Jul. 2017, doi: 10.1002/star.201600203.
1:07 muscle mass in Sout Asians [1], [2]
1:14 sarcopenia[3], [4]
1:34 brown fat?[5], [6], [7]
2:07 brown fat in infants[8]
2:31 brown fat reduces inflammation [9]
2:37 increased brown fat mass in the insulin sensitive[10]
2:42 reduced brown fat in insulin resistance[10]
2:47 anatomical locations of brown fat[11]
2:59 PET scan and MRI to image brown fat[12], [13]
3:05 infrared / thermal imaging for brown fat[14], [15]
3:38 uncoupling protein-1 (UCP-1) and brown fat[16], [17], [18]
4:00 failure to activate brown fat in south Asian upon cold exposure[19], [20]
4:19 Nutraceuticals and UCP-1 activation[21]
4:40 Rice consumption upon Latin Americans[22]
4:54 metabolic diseases among Hispanics[23], [24]
5:05 obesogenic environment[25]
5:15 pollutants and obesity[21]
7:15 Arsenic in rice[26], [27]
7:20 Arsenic & obesity and metabolic syndrome[28], [29], [30]
7:29 Arsenic deactivated brown fat[29], [31]
8:05 temperature and climate to activate brown fat [32]
10:08 diabetes reversal talk by Malaysia Kini - search for “Reverse Obesity and Type 2 Diabetes with Roczen Malaysiakini”
11:45 Gut microbiota and appendicitis[33]
12:00 lean / thin people have higher brown fat[11]
12:15 brown fat is inversely proportional to visceral fat[34], [35]
12:25 UCP-1 could be switched on[36], [37], [38]
13:10 Aborigines in New Zealand and heart attack genes, calcification [39], [40], [41]
13:28 Nattokinase, fermented food consumption [42]
13:48 Vitamin D3 absorption is better when vitamin K2 and K7 is adequate[43], [44]
13:58 Gut microbiome and ischemic heart diseases[45], [46]
18:14 Rebound with GLP-1[47], [48]
18:28 GLP-1 is a secretin[49]
18:35 Hyperinsulinemic states and mortality[50]
22:06 palm oil boiling point and aldehyde production[51], [52]
22:18 Virgin olive oil cooking and aldehyde production[53], [54]
22:30 seed / vegetable oils and aldehyde production[53], [54]
23:30 Vit A,E, CoQ10 in red palm oil is underutilized in preventive cardiology[55], [56]
28:33 Insulin resistance, sensitivity calculation. HOMA-IR, HOMA-2B[57]
28:48 Triglyceride-Glucose index[58]
29:02 UTM Diabetes subcluster preprint - “Subclustering of Type 2 Diabetes for Better Personalisation Treatment Management Using K-Means Clustering Algorithm”
29:26 Precision diabetes management according to subclusters[59], [60]
31:34 China 7 diabetes clusters and 5 clusters in Japan [61], [62]
31:52 Type 1.5 Diabetes, LADA, Autoimmune diabetes[63]
32:20 Fructose toxicity in diabetes[64], [65]
32:46 exogenous, injectable insulin cost and healthcare burden[66], [67], [68], [69]
32:55 SLGT 2 inhibitors and cardioprotection[70]
33:34 Resistant starch type 3 on starch / rice [66]
33:48 Resistant starch type 5: Lipid-Amylose complex [71]
Great discussion.
I can watch this for hours. Padat dgn info dan kajian.
Hope you get spoiled more with the uploaded references 😂
Though Dr Bhuwan is very knowledgeable and his intentions are very very good, i find this podcast is abit all over the place and hard to follow. But i guess some people need these kinds of podcasts.
For me its simple, no processed food, LOW sugar, eat in moderation. This is simple & fit for all.
Talking about genetics and all that makes it so complicated more than it is.
Why atuk nenek eat so much rice yet not so much problem.. SUGAR, PROCESSED FOOD.
first time dengar pasal brown fat ...best²
[1] A. Misra et al., “Body fat, metabolic syndrome and hyperglycemia in South Asians,” J Diabetes Complications, vol. 32, no. 11, pp. 1068-1075, Nov. 2018, doi: 10.1016/j.jdiacomp.2018.08.001.
[2] E. Pomeroy, V. Mushrif-Tripathy, T. J. Cole, J. C. K. Wells, and J. T. Stock, “Ancient origins of low lean mass among South Asians and implications for modern type 2 diabetes susceptibility,” Sci Rep, vol. 9, no. 1, p. 10515, Jul. 2019, doi: 10.1038/s41598-019-46960-9.
[3] C. Salom Vendrell, E. García Tercero, J. B. Moro Hernández, and B. A. Cedeno-Veloz, “Sarcopenia as a Little-Recognized Comorbidity of Type II Diabetes Mellitus: A Review of the Diagnosis and Treatment,” Nutrients, vol. 15, no. 19, p. 4149, Sep. 2023, doi: 10.3390/nu15194149.
[4] H. Chen, X. Huang, M. Dong, S. Wen, L. Zhou, and X. Yuan, “The Association Between Sarcopenia and Diabetes: From Pathophysiology Mechanism to Therapeutic Strategy,” Diabetes, Metabolic Syndrome and Obesity, vol. Volume 16, pp. 1541-1554, May 2023, doi: 10.2147/DMSO.S410834.
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