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BackgroundThe 2018 World Cancer Research Fund/American Institute for Cancer Research (WCRF/AICR) 3rd expert report highlights up-to-date Cancer Prevention Recommendations that may reduce burdens of many chronic diseases, including diabetes. This study examined if following a lifestyle that aligns with the recommendations - assessed via the 2018 WCRF/AICR Score - was associated with lower risk of type 2 diabetes in high-risk adults participating in the Diabetes Prevention Program Outcomes Study (DPPOS).MethodsThe Diabetes Prevention Program (DPP) randomized adults at high risk for diabetes to receive a lifestyle intervention (ILS), metformin (MET) or a placebo (PLB) (mean: 3.2 years), with additional follow-up in DPPOS for 11 years (mean: 15 years total). 2018 WCRF/AICR Scores included seven components: body weight, physical activity, plant-based foods, fast foods, red and processed meat, sugar-sweetened beverages, and alcohol; the optional breastfeeding component was excluded. Scores ranged 0-7 points (with greater scores indicating greater alignment with the recommendations) and were estimated at years 0, 1, 5, 6, 9, and 15 (N=3,147). Fasting glucose and HbA1c were measured every six months and oral glucose tolerance tests were performed annually. Adjusted Cox proportional hazard ratios (HRs) and 95% confidence intervals (CIs) were used to examine the association of both Score changes from years 0-1 and time-dependent Score changes on diabetes risk through DPP and year 15.ResultsScores improved within all groups over 15 years (p

The evolution of SARS-CoV-2 during the COVID-19 pandemic has raised interest in evolving disease manifestation and associated severity since early reports of its emergence in December 2019 (1). As SARS-CoV-2 [...]

Sex hormone binding globulin (SHBG) levels are reported to be inversely associated with diabetes risk. It is unknown whether diabetes prevention interventions increase SHBG and whether resultant changes in SHBG affect diabetes risk. The purpose of this analysis was to determine whether intensive lifestyle intervention (ILS) or metformin changed circulating SHBG and if resultant changes influenced diabetes risk in the Diabetes Prevention Program (DPP). This is a secondary analysis from the DPP (1996-2001), a randomized trial of ILS or metformin versus placebo on diabetes risk over a mean follow-up of 3.2 years. The DPP was conducted across 27 academic study centers in the USA. Men, premenopausal and postmenopausal women without hormone use in the DPP were evaluated. The DPP included overweight/obese persons with elevated fasting glucose and impaired glucose tolerance. Main outcomes measures were changes in SHBG levels at 1 year and risk of diabetes over 3 years. ILS resulted in significantly higher increases (postmenopausal women: p

OBJECTIVE: To assess associations between distal symmetric polyneuropathy (DSPN) and Diabetes Prevention Program (DPP) treatment groups, diabetes status or duration, and cumulative glycemic exposure approximately 21 years after DPP randomization. RESEARCH DESIGN AND METHODS: In the DPP, 3,234 adults ≥25 years old at high risk for diabetes were randomized to an intensive lifestyle (ILS), metformin, or placebo intervention to prevent diabetes. After the DPP ended, 2,779 joined the Diabetes Prevention Program Outcomes Study (DPPOS). Open-label metformin was continued, placebo was discontinued, ILS was provided in the form of semiannual group-based classes, and all participants were offered quarterly lifestyle classes. Symptoms and signs of DSPN were assessed in 1,792 participants at DPPOS year 17. Multivariable logistic regression models were used to evaluate DSPN associations with treatment group, diabetes status/duration, and cumulative glycemic exposure. RESULTS: At 21 years after DPP randomization, 66% of subjects had diabetes. DSPN prevalence did not differ by initial DPP treatment assignment (ILS 21.5%, metformin 21.5%, and placebo 21.9%). There was a significant interaction between treatment assignment to ILS and age (P < 0.05) on DSPN. At DPPOS year 17, the odds ratio for DSPN in comparison with ILS with placebo was 17.4% (95% CI 3.0, 29.3) lower with increasing 5-year age intervals. DSPN prevalence was slightly lower for those at risk for diabetes (19.6%) versus those with diabetes (22.7%) and was associated with longer diabetes duration and time-weighted HbA1c (P values <0.001). CONCLUSIONS: The likelihood of DSPN was similar across DPP treatment groups but higher for those with diabetes, longer diabetes duration, and higher cumulative glycemic exposure. ILS may have long-term benefits on DSPN for older adults. [ABSTRACT FROM AUTHOR]

Context: Obesity and diabetes are established risk factors for severe SARS-CoV-2 outcomes, but less is known about their impact on susceptibility to COVID-19 infection and general symptom severity. Objective: We hypothesized that those with obesity or diabetes would be more likely to self-report a positive SARS-CoV-2 test, and, among those with a positive test, have greater symptom severity and duration. Methods: Among 44 430 COVID-19 Community Research Partnership participants, we evaluated the association of self-reported and electronic health record obesity and diabetes with a self-reported positive COVID-19 test at any time. Among the 2663 participants with a self-reported positive COVID-19 test during the study, we evaluated the association of obesity and diabetes with self-report of symptom severity, duration, and hospitalization. Logistic regression models were adjusted for age, sex, race/ethnicity, socioeconomic status, and health care worker status. Results: We found a positive graded association between body mass index (BMI) category and positive COVID-19 test (overweight odds ratio [OR] 1.14 [1.05-1.25]; obesity I OR 1.29 [1.17-2.42]; obesity II OR 1.34 [1.19-1.50]; obesity III OR 1.53 [1.35-1.73]), and a similar but weaker association with COVID-19 symptoms and severity among those with a positive test. Diabetes was associated with COVID-19 infection but not symptoms after adjustment, with some evidence of an interaction between obesity and diabetes. Conclusion: While the limitations of this health system convenience sample include generalizability and selection around test seeking, the strong graded association of BMI and diabetes with self-reported COVID-19 infection suggests that obesity and diabetes may play a role in risk for symptomatic SARS-CoV-2 beyond co-occurrence with socioeconomic factors. [ABSTRACT FROM AUTHOR]

Background: Face masks have been recommended to reduce SARS‐CoV‐2 transmission. However, evidence of the individual benefit of face masks remains limited, including by vaccination status. Methods: As part of the COVID‐19 Community Research Partnership cohort study, we performed a nested case–control analysis to assess the association between self‐reported consistent mask use during contact with others outside the household and subsequent odds of symptomatic SARS‐CoV‐2 infection (COVID‐19) during November 2020–October 2021. Using conditional logistic regression, we compared 359 case‐participants to 3544 control‐participants who were matched by date, adjusting for enrollment site, age group, sex, race/ethnicity, urban/rural county classification, and healthcare worker occupation. Results: COVID‐19 was associated with not consistently wearing a mask (adjusted odds ratio [aOR] 1.49; 95% confidence interval [CI] [1.14, 1.95]). Compared with persons ≥14 days after mRNA vaccination who also reported always wearing a mask, COVID‐19 was associated with being unvaccinated (aOR 5.94; 95% CI [3.04, 11.62]), not wearing a mask (aOR 1.62; 95% CI [1.07, 2.47]), or both unvaccinated and not wearing a mask (aOR 9.07; 95% CI [4.81, 17.09]). Conclusions: Our findings indicate that consistent mask wearing can complement vaccination to reduce the risk of COVID‐19. [ABSTRACT FROM AUTHOR]

Objective: The extent to which weight loss contributes to increases in insulin sensitivity (IS) and β-cell function after surgical or medical intervention has not been directly compared in individuals with impaired glucose tolerance or newly diagnosed type 2 diabetes.Methods: The Restoring Insulin Secretion (RISE) Study included adults in the Beta-Cell Restoration Through Fat Mitigation Study (n = 88 randomized to laparoscopic gastric banding or metformin [MET]) and the Adult Medication Study (n = 267 randomized to placebo, MET, insulin glargine/MET, or liraglutide + MET [L + M]). IS and β-cell responses were measured at baseline and after 12 months by modeling of oral glucose tolerance tests and during arginine-stimulated hyperglycemic clamps. Linear regression models assessed differences between and within treatments over time.Results: BMI decreased in all treatment groups, except placebo, at 12 months. IS increased in all arms except placebo and was inversely correlated with changes in BMI. L + M was the only treatment arm that enhanced multiple measures of β-cell function independent of weight loss. Insulin secretion decreased in the laparoscopic gastric banding arm proportional to increases in IS, with no net benefit on β-cell function.Conclusions: Reducing demand on the β-cell by improving IS through weight loss does not reverse β-cell dysfunction. L + M was the only treatment that enhanced β-cell function. [ABSTRACT FROM AUTHOR]

Introduction: Observational studies of SARS-CoV-2 vaccine effectiveness depend on accurate ascertainment of vaccination receipt, date, and product type. Self-reported vaccine data may be more readily available to and less expensive for researchers than assessing medical records. Methods: We surveyed adult participants in the COVID-19 Community Research Partnership who had an authenticated Electronic Health Record (EHR) (N = 41,484) concerning receipt of SARS-CoV-2 vaccination using a daily survey beginning in December 2020 and a supplemental survey in September–October 2021. We compared self-reported information to that available in the EHR for the following data points: vaccine brand, date of first dose, and number of doses using rates of agreement and Bland–Altman plots for visual assessment. Self-reported data was available immediately following vaccination (in the daily survey) and at a delayed interval (in a secondary supplemental survey). Results: For the date of first vaccine dose, self-reported "immediate" recall was within ±7 days of the date reported in the "delayed" survey for 87.9% of participants. Among the 19.6% of participants with evidence of vaccination in their EHR, 95% self-reported vaccination in one of the two surveys. Self-reported dates were within ±7 days of documented EHR vaccination for 97.6% of the "immediate" surveys and 92.0% of the "delayed" surveys. Self-reported vaccine product details matched those in the EHR for over 98% of participants for both "immediate" and "delayed" surveys. Conclusions: Self-reported dates and product details for COVID-19 vaccination can be a good surrogate when medical records are unavailable in large observational studies. A secondary confirmation of dates for a subset of participants with EHR data will provide internal validity. [ABSTRACT FROM AUTHOR]

Introduction: The COVID-19 Community Research Partnership is a population-based longitudinal syndromic and sero-surveillance study. The study includes over 17,000 participants from six healthcare systems in North Carolina who submitted over 49,000 serology results. The purpose of this study is to use these serology data to estimate the cumulative proportion of the North Carolina population that has either been infected with SARS-CoV-2 or developed a measurable humoral response to vaccination. Methods: Adult community residents were invited to participate in the study between April 2020 and February 2021. Demographic information was collected and daily symptom screen was completed using a secure, HIPAA-compliant, online portal. A portion of participants were mailed kits containing a lateral flow assay to be used in-home to test for presence of anti-SARS-CoV-2 IgM or IgG antibodies. The cumulative proportion of participants who tested positive at least once during the study was estimated. A standard Cox proportional hazards model was constructed to illustrate the probability of seroconversion over time up to December 20, 2020 (before vaccines available). A separate analysis was performed to describe the influence of vaccines through February 15, 2021. Results: 17,688 participants contributed at least one serology result. 68.7% of the population were female, and 72.2% were between 18 and 59 years of age. The average number of serology results submitted per participant was 3.0 (±1.9). By December 20, 2020, the overall probability of seropositivity in the CCRP population was 32.6%. By February 15, 2021 the probability among healthcare workers and non-healthcare workers was 83% and 49%, respectively. An inflection upward in the probability of seropositivity was demonstrated around the end of December, suggesting an influence of vaccinations, especially for healthcare workers. Among healthcare workers, those in the oldest age category (60+ years) were 38% less likely to have seroconverted by February 15, 2021. Conclusions: Results of this study suggest more North Carolina residents may have been infected with SARS-CoV-2 than the number of documented cases as determined by positive RNA or antigen tests. The influence of vaccinations on seropositivity among North Carolina residents is also demonstrated. Additional research is needed to fully characterize the impact of seropositivity on immunity and the ultimate course of the pandemic. [ABSTRACT FROM AUTHOR]

Context: There is little information about fatty liver in prediabetes as it transitions to early diabetes.Objective: This study is aimed at evaluating the prevalence and determinants of fatty liver in the Diabetes Prevention Program (DPP).Methods: We measured liver fat as liver attenuation (LA) in Hounsfield units (HU) in 1876 participants at ~14 years following randomization into the DPP, which tested the effects of lifestyle or metformin interventions versus standard care to prevent diabetes. LA was compared among intervention groups and in those with versus without diabetes, and associations with baseline and follow-up measurements of anthropometric and metabolic covariates were assessed.Results: There were no differences in liver fat between treatment groups at 14 years of follow-up. Participants with diabetes had lower LA (mean ± SD: 46 ± 16 vs 51 ± 14 HU; P < 0.001) and a greater prevalence of fatty liver (LA < 40 HU) (34% vs 17%; P < 0.001). Severity of metabolic abnormalities at the time of LA evaluation was associated with lower LA categories in a graded manner and more strongly in those with diabetes. Averaged annual fasting insulin (an index of insulin resistance [OR, 95% CI 1.76, 1.41-2.20]) waist circumference (1.63, 1.17-2.26), and triglyceride (1.42, 1.13-1.78), but not glucose, were independently associated with LA < 40 HU prevalence.Conclusion: Fatty liver is common in the early phases of diabetes development. The association of LA with insulin resistance, waist circumference, and triglyceride levels emphasizes the importance of these markers for hepatic steatosis in this population and that assessment of hepatic fat in early diabetes development is warranted. [ABSTRACT FROM AUTHOR]

Objective: To identify predictors of glycemic worsening among youth and adults with impaired glucose tolerance (IGT) or recently diagnosed type 2 diabetes in the Restoring Insulin Secretion (RISE) Study.Research Design and Methods: A total of 91 youth (10-19 years) were randomized 1:1 to 12 months of metformin (MET) or 3 months of glargine, followed by 9 months of metformin (G-MET), and 267 adults were randomized to MET, G-MET, liraglutide plus MET (LIRA+MET), or placebo for 12 months. All participants underwent a baseline hyperglycemic clamp and a 3-h oral glucose tolerance test (OGTT) at baseline, month 6, month 12, and off treatment at month 15 and month 21. Cox models identified baseline predictors of glycemic worsening (HbA1c increase ≥0.5% from baseline).Results: Glycemic worsening occurred in 17.8% of youth versus 7.5% of adults at month 12 (P = 0.008) and in 36% of youth versus 20% of adults at month 21 (P = 0.002). In youth, glycemic worsening did not differ by treatment. In adults, month 12 glycemic worsening was less on LIRA+MET versus placebo (hazard ratio 0.21, 95% CI 0.05-0.96, P = 0.044). In both age-groups, lower baseline clamp-derived β-cell responses predicted month 12 and month 21 glycemic worsening (P < 0.01). Lower baseline OGTT-derived β-cell responses predicted month 21 worsening (P < 0.05). In youth, higher baseline HbA1c and 2-h glucose predicted month 12 and month 21 glycemic worsening, and higher fasting glucose predicted month 21 worsening (P < 0.05). In adults, lower clamp- and OGTT-derived insulin sensitivity predicted month 12 and month 21 worsening (P < 0.05).Conclusions: Glycemic worsening was more common among youth than adults with IGT or recently diagnosed type 2 diabetes, predicted by lower baseline β-cell responses in both groups, hyperglycemia in youth, and insulin resistance in adults. [ABSTRACT FROM AUTHOR]

Objective: To compare effects of medications and laparoscopic gastric band surgery (LB) on α-cell function in dysglycemic youth and adults in the Restoring Insulin Secretion (RISE) Study protocols.Research Design and Methods: Glucagon was measured in three randomized, parallel, clinical studies: 1) 91 youth studied at baseline, after 12 months on metformin alone (MET) or glargine followed by metformin (G/M), and 3 months after treatment withdrawal; 2) 267 adults studied at the same time points and treated with MET, G/M, or liraglutide plus metformin (L+M) or given placebo (PLAC); and 3) 88 adults studied at baseline and after 12 and 24 months of LB or MET. Fasting glucagon, glucagon suppression by glucose, and acute glucagon response (AGR) to arginine were assessed during hyperglycemic clamps. Glucagon suppression was also measured during oral glucose tolerance tests (OGTTs).Results: No change in fasting glucagon, steady-state glucagon, or AGR was seen at 12 months following treatment with MET or G/M (in youth and adults) or PLAC (in adults). In contrast, L+M reduced these measures at 12 months (all P ≤ 0.005), which was maintained 3 months after treatment withdrawal (all P < 0.01). LB in adults also reduced fasting glucagon, steady-state glucagon, and AGR at 12 and 24 months (P < 0.05 for all, except AGR at 12 months [P = 0.098]). Similarly, glucagon suppression during OGTTs was greater with L+M and LB. Linear models demonstrated that treatment effects on glucagon with L+M and LB were largely associated with weight loss.Conclusions: Glucagon concentrations were reduced by L+M and LB in adults with dysglycemia, an effect principally attributable to weight loss in both interventions. [ABSTRACT FROM AUTHOR]

Objective: To determine whether β-cell hyperresponsiveness and insulin resistance in youth versus adults in the Restoring Insulin Secretion (RISE) Study are related to increased glucagon release.Research Design and Methods: In 66 youth and 350 adults with impaired glucose tolerance (IGT) or recently diagnosed type 2 diabetes (drug naive), we performed hyperglycemic clamps and oral glucose tolerance tests (OGTTs). From clamps we quantified insulin sensitivity (M/I), plasma fasting glucagon and C-peptide, steady-state glucagon and C-peptide at glucose of 11.1 mmol/L, and arginine-stimulated glucagon (acute glucagon response [AGR]) and C-peptide (ACPRmax) responses at glucose >25 mmol/L.Results: Mean ± SD fasting glucagon (7.63 ± 3.47 vs. 8.55 ± 4.47 pmol/L; P = 0.063) and steady-state glucagon (2.24 ± 1.46 vs. 2.49 ± 1.96 pmol/L, P = 0.234) were not different in youth and adults, respectively, while AGR was lower in youth (14.1 ± 5.2 vs. 16.8 ± 8.8 pmol/L, P = 0.001). Significant age-group differences in insulin sensitivity, fasting C-peptide, steady-state C-peptide, and ACPRmax were not related to glucagon. Fasting glucose and glucagon were positively correlated in adults (r = 0.133, P = 0.012) and negatively correlated in youth (r = -0.143, P = 0.251). In both age-groups, higher fasting glucagon was associated with higher fasting C-peptide (youth r = 0.209, P = 0.091; adults r = 0.335, P < 0.001) and lower insulin sensitivity (youth r = -0.228, P = 0.066; adults r = -0.324, P < 0.001). With comparable fasting glucagon, youth had greater C-peptide and lower insulin sensitivity. OGTT suppression of glucagon was greater in youth.Conclusions: Youth with IGT or recently diagnosed type 2 diabetes (drug naive) have hyperresponsive β-cells and lower insulin sensitivity, but their glucagon concentrations are not increased compared with those in adults. Thus, α-cell dysfunction does not appear to explain the difference in β-cell function and insulin sensitivity in youth versus adults. [ABSTRACT FROM AUTHOR]

Objectives. The purpose of the study was to determine whether breast-feeding is associated with increased longevity or cause-specific survival. Methods. Teachers throughout California identified intellectually gifted children as part of a prospective study begun in the 1920s by Lewis Terman. Information on breast-feeding was available on 1170 subjects, who have been followed for more than 65 years. Results. Survival analysis (Cox proportional hazards model) indicated that breast-feeding was associated with increased longevity, even after adjustment for age at baseline, birthweight, infant health, and childhood socioeconomic status, but only among men, and the association was not significant (P = .15). Neither cardiovascular disease nor cancer survival was significantly associated with duration of breast-feeding for either sex. Survival from deaths due to injuries was positively associated with breast-feeding after adjustment (P = .03) and demonstrated a clear gradient with duration, but only among men. Conclusions. Overall, the present study does not provide strong evidence that breast-feeding is associated with adult longevity. The reduced risk of death from injury may reflect chance, in that the association was significant only for men, or it may reflect psychosocial correlates of breast-feeding practices. (Am J Public Health. 1994;84:1458-1462), Breast feeding infants may have some affect on their long-term survival, especially for males. An analysis of data from the Terman Life Cycle Study focused on participants born between 1904 and 1915. The Terman project surveyed gifted, mostly white, mostly middle-class children in California and followed them until 1986. The analysis of breast feeding and survival included 647 males and 523 females. Of these, 115 were never breast-fed. The average length of breast feeding was eight months for the 1,155 who were breast-fed for some period. The children who were breast-fed were healthier infants, with the effect increasing with the length of time they were breast-fed. When mortality rates were analyzed as of 1986, 449 subjects had died. Although overall mortality rates were higher for men than women, they were lower for men who had been breast-fed than for men who had not. This difference was not present for the women. Breast feeding seemed to have little effect on most specific causes of death or survival of specific illnesses. However, both men and women who had been breast-fed had lower rates of death from injury. This was significant for men and the benefit increased with the length of breast feeding.

Drinking caffeinated coffee may be associated with decreased bone density in elderly women. Researchers used survey data of 980 postmenopausal women with an average age of 73 years to evaluate the relation between caffeinated coffee, milk consumption and bone mineral density. Eighty-eight percent of the women reported drinking coffee regularly at some point in their lives and 53% reported current daily coffee consumption. Smoking and alcohol use were significantly associated with lifetime coffee use. Bone mineral density of the hip and spine decreased substantially with increasing years of caffeinated coffee use. The decrease was significant, independent of age, bone mass index, cigarette and alcohol use, exercise, diuretic and estrogen use, number of live births and years since menopause. Lifetime coffee use was associated with bone density reductions only among women who did not drink at least one glass of milk per day between age 20 and 50 years., Objective.--To describe the association of lifetime intake of caffeinated coffee, in cup-years, to bone mineral density (BMD) of the hip and spine in postmenopausal women; and to determine the effect of regular milk intake on this association. Design.--Women from an established epidemiologic cohort had measures of BMD and gave a medical and behavioral history that included caffeinated coffee and daily milk intake between the ages of 12 and 18 years, 20 and 50 years, and 50 years of age and older. Setting.--A community-based population of older women, Rancho Bernardo, Calif. Participants.--All 980 postmenopausal women aged 50 to 98 years (mean age, 72.7 years) who participated between 1988 and 1991. Main Outcome Measures.--Bone density at the hip and lumbar spine measured by dual energy x-ray absorptiometry. Main Results.--There was a statistically significant graded association between increasing lifetime intake of caffeinated coffee and decreasing BMD at both the hip and spine, independent of age, obesity, parity, years since menopause, and the use of tobacco, alcohol, estrogen, thiazides, and calcium supplements. Bone density did not vary by lifetime coffee intake in women who reported drinking at least one glass of milk per day during most of their adult lives. Conclusions.--Lifetime caffeinated coffee intake equivalent to two cups per day is associated with decreased bone density in older women who do not drink milk on a daily basis. (JAMA. 1994;271:280-283)

objectives. The association between cigarette smoking and bone mineral density was examined prospectively in a population-based study of older Caucasian men and women. Methods. Smoking patterns were determined at a 1972-1974 baseline evaluation and, again, 16 years later when 544 men and 822 women had bone mineral density measurements taken. Results. Men and women who were cigarette smokers at baseline demonstrated significantly reduced bone mineral density of the hip compared with nonsmokers. Baseline smoking was not associated with significantly lower bone density at non-hip sites. Women demonstrated a significant dose - response relationship between baseline smoking status at all hip sites measured. Both sexes exhibited significant dose-response relationships between hip bone mineral density and change in smoking status between baseline and follow-up, demonstrating that smoking cessation in later life was beneficial in halting bone density loss associated with smoking. Conclusions. Smoking was positively and significantly associated with decreased hip bone mineral density in old age. Bone loss associated with smoking would be expected to predict an increased risk of hip fracture in those who do not succumb earlier to another complication of tobacco use. (Am J Public Health. 1993;83:1265-1270), A history of smoking is a significant predictor of decreased hip bone density in older white people. A group of men and women were evaluated in a 1972-74 baseline study in which smoking habits were assessed. Sixteen years later, 822 women and 544 men over age 60 were reevaluated. The follow-up study showed that smoking for 16-18 years is associated with significant osteopenia (reduced bone mass) in the hip. The more cigarettes men and women smoked, the more bone mass was reduced. Women especially showed reduced bone density at three different sites on the hip which varied directly with number of cigarettes smoked. This so-called dose-response relationship between bone mass and cigarettes smoked suggests that quitting smoking, even later in life, might help to preserve bone density.

Premenopausal women have far lower mortality from heart disease than men do in Western societies. However, the reverse is true for adult non-insulin-dependent diabetics, and women are now at greater risk than male diabetics for fatal ischemic heart disease (in which blood flow to the heart is impeded by blocked arteries). The Rancho Bernardo (California) study of older, upper-middle-class, white residents measured risk factors for heart disease. The follow-up now extends to 14 years. Of the original population, 207 men and 127 women had diabetes. Hyperglycemia (excessive levels of blood sugar) does not entirely explain the risk of heart disease for men or women. It has been suggested that diabetic women have lower levels of high density lipoprotein (HDL, the so-called 'good cholesterol') than diabetic men, and are thus at increased risk, but this factor does not explain the difference in mortality. The question arises whether the increased risk is a statistical artifact relating to the low risk of women without diabetes, or a result of the deleterious effects of diabetes in women. The former seems more likely. Evidence also points to an insulin-androgen (a male hormone) interaction. Women with a male pattern of fat (central obesity, or a 'paunch') have a poor cholesterol profile and increased risk of heart disease. In another study, the waist-to-hip ratio was the strongest predictor of HDL level. Studies point to a relationship between androgens and excess insulin in the blood, as well as higher levels of triglyceride (a fat) and lower HDL cholesterol levels. The Rancho Bernardo study suggests that diabetes increases the probability of developing heart disease for women, and outweighs their usual lower risk. This risk is not affected by the usual heart disease risk factors. (Consumer Summary produced by Reliance Medical Information, Inc.)

One group of factors important in determining the response to trauma are so-called 'host factors', such as age, sex, and pre-existing disease of the patient. Since the relationship between pre-existing disease and mortality after trauma has not been determined, these factors were investigated for 3,074 people who died following trauma in California in 1983. Computerized hospital discharge records were analyzed, which contained demographic information as well as information about the hospitalization, diagnoses, and procedures. Two computed scores were used for each patient to express the severity of trauma. Each trauma victim (a case) was statistically matched with, at most, four survivors of similar episodes who had been discharged from the same hospital and were of similar age (controls; 9,869 were studied). Cases and controls were then compared to determine the incidence of preexisting conditions (PECs). Eleven of these, including hypertension (high blood pressure), diabetes, chronic liver disease, obesity, and others, were singled out for analysis. Results showed that 59 percent of the deaths occurred among patients 55 years old or older, and that nearly three fourths of the deaths were due to trauma of relatively minor severity, most involving hip fractures. Patients with one or more of the 11 PECs were 30 percent more likely to die than those without PECs; with two or more PECs, they were 60 percent more likely. The PECs that had the most effect on risk of dying after trauma were cirrhosis of the liver (a chronic condition) and congenital coagulation defects (disorders of blood clotting present from birth), but chronic obstructive pulmonary disease (a lung disorder), ischemic heart disease (inadequate blood supply to the heart), and diabetic patients, still had an increased risk. It was interesting that trauma victims with hypertension or psychoses were less likely to die than patients without. PEC prevalence for California hospital admissions is provided. The effect of PECs on mortality was greatest among patients with mild or moderate injury; for the rest, it varied with age of the patient, being least for the oldest patients (due to the method of analysis: these patients already had a high risk of dying). The findings suggest that PECs contribute to increased risk for all patients suffering moderate trauma, and that the adult aged 45 to 54 is at increased risk after injury of any severity. They suggest further that the PECs found important here should be taken into account in triage (classification and decision about treatment) of trauma patients. (Consumer Summary produced by Reliance Medical Information, Inc.)