scholarly journals Low-carbohydrate–high-protein diet and long-term survival in a general population cohort

2006 ◽  
Vol 61 (5) ◽  
pp. 575-581 ◽  
Author(s):  
A Trichopoulou ◽  
T Psaltopoulou ◽  
P Orfanos ◽  
C-C Hsieh ◽  
D Trichopoulos
Keyword(s):  
General Population ◽  
High Protein Diet ◽  
High Protein ◽  
Protein Diet ◽  
Term Survival ◽  
Long Term Survival ◽  
Population Cohort ◽  
Low Carbohydrate ◽  
General Population Cohort

scholarly journals Long Term Metabolic and Health Effects of a Low-Carbohydrate, High-Fat, High-Protein Diet in Mus musculus: A Nineteen Week Longitudinal Study

2005 ◽  
Vol 4 (1) ◽  
Author(s):  
Donald Harris ◽  
Christopher Bell ◽  
Misty Retzlaff ◽  
Stephanie Toering ◽  
Elizabeth Wurdak ◽  
...  
Keyword(s):  
Health Effects ◽  
High Protein Diet ◽  
Liver Glycogen ◽  
High Protein ◽  
Protein Diet ◽  
Control Group ◽  
Tissue Analysis ◽  
High Fat ◽  
Low Carbohydrate

This study was designed to investigate the long-term metabolic adaptations and health effects of a low-carbohydrate, high-fat/protein diet in mice. One-month-old male ICR mice were fed a control, conventional high-carbohydrate diet (n=21) or an experimental low-carbohydrate, high-fat, high-protein diet (n=20). One pair of mice per group was euthanized at two-week intervals for five months for tissue analysis. Basic metabolic data, body and tissue weights, blood and plasma metabolite and lipid profiles, liver glycogen and protein content, and liver serine dehydratase and glucose-6-phosphate dehydrogenase activities were analyzed. The low-carbohydrate group gained significantly more weight (p<0.005 after 4 weeks) than the normally growing control group. Although ketosis was initially stimulated in the low-carbohydrate group, enzyme and tissue analysis suggest that gluconeogenic activity was sufficient to alleviate the effects of severe dietary carbohydrate restriction and allow for glucose metabolism close to that demonstrated in the control group.

scholarly journals Does long-term creatine supplementation impair kidney function in resistance-trained individuals consuming a high-protein diet?

2013 ◽  
Vol 10 (1) ◽  
pp. 26 ◽  
Author(s):  
Rebeca Lugaresi ◽  
Marco Leme ◽  
Vítor de Salles Painelli ◽  
Igor Murai ◽  
Hamilton Roschel ◽  
...  
Keyword(s):  
Kidney Function ◽  
Creatine Supplementation ◽  
High Protein Diet ◽  
High Protein ◽  
Protein Diet

scholarly journals High-Protein Diet Induces Hyperuricemia in a New Animal Model for Studying Human Gout

2020 ◽  
Vol 21 (6) ◽  
pp. 2147 ◽  
Author(s):  
Fan Hong ◽  
Aijuan Zheng ◽  
Pengfei Xu ◽  
Jialin Wang ◽  
Tingting Xue ◽  
...  
Keyword(s):  
Animal Model ◽  
Metabolic Diseases ◽  
High Protein Diet ◽  
Serum Urate ◽  
Dietary Factors ◽  
High Protein ◽  
Protein Diet ◽  
Positive Effects ◽  
Biological Studies

Hyperuricemia is a central risk factor for gout and increases the risk for other chronic diseases, including cardiometabolic disease, kidney disease, and hypertension. Overproduction of urate is one of the main reasons for hyperuricemia, and dietary factors including seafoods, meats, and drinking are contributed to the development of it. However, the lack of a suitable animal model for urate metabolism is one of the main reasons for the delay and limitations of hyperuricemia research. Combining evolutionary biological studies and clinical studies, we conclude that chicken is a preferred animal model for hyperuricemia. Thus, we provided chickens a high-protein diet (HPD) to evaluate the changes in the serum urate levels in chickens. In our study, the HPD increased the serum urate level and maintained it at a long-term high level in chickens. Long-term high serum urate levels induced an abnormal chicken claw morphology and the precipitation of monosodium urate (MSU) in joint synovial fluid. In addition, a long-term HPD also decreased the glomerular filtration rate and induced mild renal injury. Most importantly, allopurinol and probenecid displayed the positive effects in decreasing serum urate and then attenuated hyperuricemia in chicken model. These findings provide a novel model for hyperuricemia and a new opportunity to further investigate the effects of long-term hyperuricemia on other metabolic diseases.

scholarly journals Endocrine and Metabolic Diseases Among Colorectal Cancer Survivors in a Population-Based Cohort

2019 ◽  
Vol 112 (1) ◽  
pp. 78-86
Author(s):  
Makenzie L Hawkins ◽  
Brenna E Blackburn ◽  
Kerry Rowe ◽  
John Snyder ◽  
Vikrant G Deshmukh ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Risk Factor ◽  
General Population ◽  
Metabolic Diseases ◽  
The United States ◽  
Population Cohort ◽  
Increased Risk ◽  
General Population Cohort ◽  
Time Periods

Abstract Background There are an estimated 1.4 million colorectal cancer (CRC) survivors in the United States. Research on endocrine and metabolic diseases over the long term in CRC survivors is limited. Obesity is a risk factor for CRC; thus it is of interest to investigate diseases that may share this risk factor, such as diabetes, for long-term health outcomes among CRC survivors. Methods A total of 7114 CRC patients were identified from the Utah Population Database and matched to a general population cohort of 25 979 individuals on birth year, sex, and birth state. Disease diagnoses (assessed over three time periods of 1–5 years, 5–10 years, and &gt;10 years) were identified using electronic medical records and statewide ambulatory and inpatient discharge data. Cox proportional hazard models were used to estimate the risk of endocrine and metabolic disease. Results Across all three time periods, risks for endocrine and metabolic diseases were statistically significantly greater for CRC survivors compared with the general population cohort. At 1–5 years postdiagnosis, CRC survivors’ risk for diabetes mellitus with complications was statistically significantly elevated (hazard ratio [HR] = 1.36, 99% confidence interval [CI] = 1.09 to 1.70). CRC survivors also experienced a 40% increased risk of obesity at 1–5 years postcancer diagnosis (HR= 1.40, 99% CI= 1.66 to 2.18) and a 50% increased risk at 5–10 years postdiagnosis (HR = 1.50, 99% CI= 1.16 to 1.95). Conclusions Endocrine and metabolic diseases were statistically significantly higher in CRC survivors throughout the follow-up periods of 1–5 years, 5–10 years, and more than 10 years postdiagnosis. As the number of CRC survivors increases, understanding the long-term trajectory is critical for improved survivorship care.

Long-Term Survival and Late Relapse in 5-Year Survivors of Allogeneic Hematopoietic-Cell Transplantation (HCT) for Chronic Myeloid Leukemia (CML) in First Chronic Phase.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 3321-3321
Author(s):  
John M. Goldman ◽  
Navneet S. Majhail ◽  
John P. Klein ◽  
Zhiwei Wang ◽  
Kathleen A. Sobocinski ◽  
...  
Keyword(s):  
General Population ◽  
Conflicts Of Interest ◽  
Chronic Gvhd ◽  
Chronic Phase ◽  
Term Survival ◽  
Long Term Survival ◽  
Late Mortality ◽  
Allogeneic Hct ◽  
Risk Of Relapse

Abstract Abstract 3321 Poster Board III-209 Prior to the advent of tyrosine kinase inhibitors, allogeneic HCT was standard therapy for CML. However, very long-term outcomes of allogeneic HCT for CML are not well described. To evaluate the probability and risk factors for late mortality and relapse in this patient population, we conducted a retrospective cohort study that included 2444 patients who received a myeloablative allogeneic HCT for CML in first chronic phase between 1978 and 1998 and had survived in continuous complete remission for at least 5 years. Relapse was considered the earliest reported date of the following: hematologic recurrence, cytogenetic recurrence or initiation of therapy for recurrence. The median followup of our cohort was 11 years (range, 5-25) from HCT; 377 patients had followup >15 years. Donor sources were HLA-matched siblings (MSD) in 1692, unrelated donors (URD) in 639 and other related donors in 113 patients. The median age at HCT was 35 years and patients primarily received bone marrow grafts (96%) and conditioning using either total-body irradiation (TBI, 61%) or BuCy (38%) regimens. Acute and chronic graft-versus-host disease (GVHD) occurred in 43% and 62% of patients, respectively. The probabilities of overall survival at 15 years were 88% (95% CI, 86-90%) for MSD and 87% (83-90%) for URD recipients. Corresponding cumulative incidences of relapse at 15 years were 8% (7-10%) and 2% (1-4%), respectively. The latest reported relapse occurred 18 years post-HCT. In multivariable analyses addressing the importance of patient, disease and transplant related factors for long-term survival, older age at HCT, use of female donor for a male recipient, use of TBI based conditioning, acute GVHD and chronic GVHD all independently increased the risk of late mortality. Chronic GVHD reduced the risk of relapse, but increased the risk of non-relapse mortality. Recipients of MSD and URD had similar risks of long-term mortality, relapse and non-relapse mortality. Compared to an age, gender and race adjusted general population, 5 year survivors of HCT for CML were 2.9 times (95% CI, 1.9-3.9) more likely to die at 6 years and 2.5 times (1.3-3.7) more likely to die at 10 years after HCT. However, by 15 years after HCT, their relatively mortality (2.3 [0-4.9]) was not significantly different than the general population. In summary, recipients of allogeneic HCT for CML in first chronic phase who remain in remission for at least 5 years after HCT have very favorable subsequent long-term survival with mortality rates eventually approaching those of the general population. There is a small but continuing risk of relapse even in these long-term survivors. Chronic GVHD protects against relapse but increases the risks of non-relapse mortality. Disclosures No relevant conflicts of interest to declare.

Incidence of second primary malignancy (SPM) in patients with mucosa-associated lymphoid tissue lymphoma (MALToma).

2020 ◽  
Vol 38 (15_suppl) ◽  
pp. e20043-e20043
Author(s):  
Nibash Budhathoki ◽  
Sunita Timilsina ◽  
Charles Thomas ◽  
Aaron Damato ◽  
Catherine S. Magid Diefenbach ◽  
...  
Keyword(s):  
At Risk ◽  
General Population ◽  
Malt Lymphoma ◽  
Lymphoid Tissue ◽  
Latency Period ◽  
Median Latency ◽  
Term Survival ◽  
Primary Tumors ◽  
Long Term Survival

e20043 Background: MALTomas are extranodal marginal zone lymphomas that arise from B cells in various mucosal lymphoid tissue and are typically indolent. Patients with MALTomas may be at risk for additional cancers due to their long-term survival following treatment, however the incidence of SPM in MALTomas in the U.S. has not been previously described. Methods: Adults with MALT lymphoma were identified using the 2000-2016 SEER-18 database. SPM was defined as tumors diagnosed ≥6 months and up to x months from lymphoma diagnosis. SEER*stat was used to calculate SPM by multiple primary standardized incidence ratio based on observed (O) and expected (E) cases. The expected cases of new cancers of specific types were estimated by assuming that incidence rates for new primary tumors corresponded to sex, age, and calendar time–specific SEER rates for similar invasive primary cancers and applying those rates to the accumulated person-years (PYR) of observation. Excess absolute risk (EAR) of malignancy per 10,000 PYR at risk was calculated as ([O − E]/PYR) × 10,000. Results: As summarized in the table, 12,500 patients were diagnosed with MALT lymphoma of which 1466 (11.8%) developed 1626 SPMs (O/E rate 1.5, 95%CI 1.4-1.5, P < 0.001, EAR 70.4). Median latency period was 54 months (range 6 - 201). Non-Hodgkin lymphomas at separate tissue sites were the most common SPM, with 299 documented cases (O/E rate 6.2, 95%CI -5.4-6.8, P < 0.001, EAR 33.4). Between 6-24 months from MALToma diagnosis, head and neck, renal cell, liver, and anal cancers were increased, while after 24 months, gastric and small bowel cancers, CLL, ALL, and myeloma were increased compared to the general population of the same age group. Conclusions: There is distinct pattern of SPM among patients with MALT lymphoma in within and after 2 years from diagnosis, with an increased incidence compared to the general population. Consider the median latency, SPM may be due in part to the long-term survival and relatively older age of this population. [Table: see text]

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