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Biomedical subjects

T D Berry

Publications and source records attributed to T D Berry.

At least 19 recordsLinked to original sources
PubMed1997

Dietary fats and colon cancer: assessment of risk associated with specific fatty acids.

There are many biological mechanisms whereby dietary fat and specific dietary fatty acids may alter risk of colon cancer in addition to their contribution to total energy intake. To evaluate these potential associations, we used detailed dietary intake data collected in a population-based study of 1,993 incident colon cancer cases and 2,410 controls conducted in 3 areas of the United States. The most commonly consumed fatty acid in the study population was oleic acid. One-third of dietary fats consumed came from additions to other foods at the table or from the preparation of other foods. After adjusting for total energy intake, physical activity and body size, neither total dietary fat nor specific fatty acids was associated with risk of colon cancer. However, among older women, fats from food preparation were associated with increased risk of colon cancer (OR 1.84, 95% CI 1.20-2.80), while fats from foods themselves or from additions to other foods were not. While dietary fats were not associated with colon cancer risk in the total population, subgroups of the population appeared to be at slightly greater risk if they consumed a high-fat diet. Women who consumed a diet high in mono-unsaturated fatty acids (MFAs) and poly-unsaturated fatty acids (PFAs) and who had a family history of colorectal cancer were at greater risk of colon cancer than those with similar intakes but without a family history of colorectal cancer. Similar associations with family history were noted among men diagnosed at younger ages for MFA, linolenic acid and 20-carbon PFA.

Adult↗
PubMed1997

Dietary energy sources and colon cancer risk.

Because energy-contributing nutrients are highly correlated with total energy, the association with colon cancer from energy versus other components of energy-providing nutrients is often not clear. Dietary data from a population-based case-control study of colon cancer were analyzed in subjects from California, Utah, and Minnesota in 1991-1994 to assess the colon cancer risk associated with consumption of energy, fat, protein, and carbohydrate. After adjustment for long-term physical activity, total energy intake increased risk of colon cancer in men (odds ratio = 1.74, 95% confidence interval 1.14-2.67 for highest vs. lowest quartile) and in women (odds ratio = 1.70, 95% confidence interval 1.07-2.70). Various methods of analysis suggested that intakes of individual sources of energy (dietary fat, protein, and carbohydrate) were not associated with colon cancer risk after total energy intake was taken into account. People who consumed a high-calorie diet that was dense in fiber and calcium appeared to be at lower risk than people with the same caloric intake who consumed smaller amounts of dietary fiber and calcium. Individuals with a first-degree relative with colorectal cancer, especially those diagnosed at a younger age, were at a greater risk from a diet high in energy than were individuals without a family history of colorectal cancer.

Adult↗
PubMed1997

Energy balance and colon cancer--beyond physical activity.

Low levels of physical activity and high levels of energy intake and body mass have all been directly associated with colon cancer. The purpose of this study was to determine how physical inactivity interacts with other components of energy balance (energy intake and body mass) in determining colon cancer risk. Data were obtained from 2073 first primary cases of colon cancer and 2466 age- and sex-matched controls identified from 8 counties in Utah, the Northern California Kaiser Permanente Medical Care Program, and the Twin Cities metropolitan area in Minnesota. Recent and lifetime physical activity was assessed by intensity of activities performed at home, leisure, and at work; energy intake was estimated from an extensive diet history questionnaire; and body mass index (BMI) was calculated from measured height at the time of interview and reported weight for the referent year. For both men and women, lack of lifetime vigorous leisure-time activity was associated with increased risk of colon cancer [odds ratio (OR), 1.63 and 95% confidence interval (CI), 1.26-2.12 for men and OR, 1.59 and 95% CI, 1.21-2.10 for women, comparing the lowest to highest level of activity]. There were no differences in risk associated with physical activity by tumor site within the colon or by age at diagnosis. High levels of energy intake were also associated with increased risk of colon cancer in men and women (OR, 1.74 and 95% CI, 1.14-2.67 for men and OR, 1.70 and 95% CI, 1.07-2.70 for women). A large BMI was more associated with increased risk in men (OR, 1.94 and 95% CI, 1.49-2.54) than in women (OR, 1.45 and 95% CI, 1.08-1.94). Those at greatest risk of colon cancer were those who had the most unfavorable energy balance in that they were physically inactive, had high energy intakes, and had a large BMI (OR, 3.35 and 95% CI, 2.09-5.35). However, when physical activity was high, having a high energy intake and large BMI resulted in a nonsignificant increased colon cancer risk (OR, 1.28 and 95% CI, 0.81-2.03). This pattern was consistent between the sexes, but there was some evidence that men may be at higher risk than women, especially older women, as a result of unfavorable energy balance. These results support previous findings that physical inactivity, high energy intake, and large body mass are associated with increased risk of developing colon cancer. However, energy balance as a whole seems to be associated with risk of colon cancer. These findings suggest systemic metabolic influences on carcinogenesis and have important implications for prevention.

Adult↗
PubMed1997

Diet diversity, diet composition, and risk of colon cancer (United States).

In this study, we evaluate diet diversity, diet composition, and risk of colon cancer in an incident population-based study of 1,993 cases and 2,410 controls in the Kaiser Permanente Medical Care Program of Northern California, eight counties in Utah, and the Twin Cities area of Minnesota (United States). Ninety-one and one-half percent of the population were non-Hispanic White. Dietary intake was obtained using an adaptation of the CARDIA diet-history questionnaire. Diet diversity was defined as the number of unique food items reported; diversity also was explored within six major food groups. Composition of the diet was described by estimating the proportion of total number of food items contributed by major food groups. Younger individuals, higher educated individuals, and those who lived in larger households reported eating the most diverse diet. Total diet diversity was not associated with colon cancer. However, eating a diet with greater diversity of meats, poultry, fish, and eggs, was associated with a 50 percent increase in risk among all men (95 percent confidence interval [CI] = 1.1-2.0; P trend = 0.01), with slightly stronger associations for younger men and men with distal tumors. A diet with a greater number of refined grain products also was associated with increased risk among men (odds ratio [OR] = 1.7, CI = 1.3-2.3). Women who ate a diet with a more diverse pattern of vegetables were at approximately a 20 percent lower risk than women who had the least diverse diet in vegetables. Assessment of diet composition showed that men who consumed a large proportion of their food items from meat, fish, poultry, and eggs were at an increased risk, with the most marked association being for distal tumors (OR = 1.7, CI = 1.2-2.5). Women who consumed the largest percentage of their food items in the form of plant foods (fruits, vegetables, or whole grains) were at a reduced risk of developing colon cancer (OR = 0.7, CI = 0.5-1.0).

Adult↗
PubMed1997

Plant foods and colon cancer: an assessment of specific foods and their related nutrients (United States).

Plant foods have been associated inversely with colon cancer. Since a major focus of this study was to identify components of plant foods which may account for their association with colon cancer, nutrients which are commonly found in plant foods also were evaluated. A population-based case-control study was conducted in Northern California, Utah, and the 'Twin Cities' area of Minnesota (United States). Complete data were available from interviewer-administered questionnaires on 1,993 cases and 2,410 controls. Higher intakes of vegetables (for highest relative to lowest quintile of intake) were associated inversely with colon cancer risk: the odds ratio (OR) was 0.7 for both men (95 percent [CI] confidence interval = 0.5-0.9) and women (CI = 0.5-1.0). Associations were stronger among those with proximal tumors. Total fruit intake was not associated with colon cancer risk although, among men, higher levels of whole grain intake were associated with a decreased risk (OR = 0.6, CI = 0.4-0.9 for older men); high intakes of refined grains were associated with an increased risk (OR = 1.5, CI = 1.1-2.1). Dietary fiber intake was associated with a decreased risk of colon cancer: OR = 0.5 (CI = 0.3-0.9) for older men; OR = 0.7 (CI = 0.4-1.2) for older women; OR = 0.6 (CI = 0.4-1.0) for men with proximal tumors; OR = 0.5 (CI = 0.3-0.9) for women with proximal tumors. Other nutrients, for which plant foods were the major contributor--such as vitamin B6, thiamin, and niacin (women only)--also were associated inversely with colon cancer. Neither beta-carotene nor vitamin C was protective for colon cancer. Adjustment of plant foods for nutrients found in plant foods or for supplement use did not appreciably alter the observed associations between plant foods and colon cancer.

Adult↗
PubMed1997

Dietary sugar and colon cancer.

It has been hypothesized that levels of triglycerides, glucose, and insulin are associated with risk of colon cancer and that diets high in simple sugars increase risk of colon cancer because of their impact on these factors. Limited epidemiological evidence supports the association between simple carbohydrates and risk of colon cancer. Using data from a population-based case-control study (n = 1993 cases and 2410 controls), we examined the associations between dietary sugars, foods containing high level of sugars, and dietary glycemic index (GI) and colon cancer. A dietary GI was developed to estimate metabolic response to a diet that may increase plasma glucose levels. Dietary data were obtained using a validated diet history questionnaire. High levels of sucrose intake were associated with increased risk of colon cancer among younger men [odds ratio (OR) for highest quintile relative to lowest, 1.59; 95% confidence interval (CI), 1.07-2.37]. There was also a trend of increasing colon cancer risk associated with a higher sucrose:dietary ratio for proximal tumors in both men and women. Individuals with proximal tumors who consumed a diet ranked as having a high GI were at increased risk (for men, comparing highest quintile to lowest quintile: OR, 1.58; 95% CI, 1.06-2.36; P trend 0.04; for women: OR, 1.72; 95% CI, 1.11-2.67; P trend 0.04). Those at greatest risk from a high dietary GI were those who were sedentary (for men, relative to those who were most active and had a low-GI diet: OR, 3.46; 95% CI, 1.78-6.70; for women: OR, 2.00; 95% CI, 0.98-4.07). We also observed that people who had a high sucrose: dietary fiber ration and who also were sedentary and had a large body mass index were at increased risk (OR, 4.58; 95% CI, 2.33-8.98) relative to those who had a low sucrose:dietary fiber ratio, were active, and had low body mass indices. These findings support previous reports that dietary sugars, especially diet high in simple carbohydrates relative to complex carbohydrates, increase risk of colon cancer, possibly through their impact on plasma glucose levels.

Adult↗
PubMed1994

Objective system for interviewer performance evaluation for use in epidemiologic studies.

In this paper, the authors present an objective system to evaluate interviewer performance for use in epidemiologic studies. With this quality control system, all study interviews are audio-taped, and a random sample of interviews are coded according to interviewer behaviors, such as whether the interviewer asked the questions exactly as written and used the probes appropriately. With the use of data obtained from a large case-control study of colon cancer, the authors observed that 94.2% of all questions were asked in the same manner by all interviewers and that 89.5% of all probing behaviors were appropriate. They show that questions that required additional interviewer behaviors were more likely to result in variation in response that can be attributed to the interviewer. These findings have implications for study design and interpretation of study results. From simulations, the authors have estimated the impact of uncorrected interviewer variability on study power and ability to detect disease associations. Uncorrected interviewer variability could decrease study power from 84% to 56%. From simulations, the authors observed that odds ratios could be biased downward from 1.8 to 1.3. These findings illustrate the importance of using a continuous quality control program in epidemiologic research.

Epidemiologic Methods↗
PubMed1994

A computerized diet history questionnaire for epidemiologic studies.

OBJECTIVE: To describe methods used to computerize the diet history questionnaire developed for the Coronary Artery Risk Factor Development in Young Adult (CARDIA) study and to describe quality-control procedures used in conjunction with dietary assessment. DESIGN: The computerized diet history is being used in a case-control study. Because of the computerized nature of the questionnaire, we developed quality-control procedures that incorporate listening to an audiotape of the interview while visually reviewing recorded data. SETTING: Three centers involved in a population-based epidemiologic study of colon cancer. SUBJECTS: Men and women between the ages of 30 and 79 years. RESULTS: Quality-control results showed that 100% of the computerized forms would be free of errors if the data were subjected to visual review only. Probing errors, which accounted for 47.3% of all errors, were the most commonly encountered errors. In probing errors the interviewer did not probe in a nondirective manner, or the interviewer failed to verify responses that might be considered questionable. APPLICATIONS: The CARDIA diet history was computerized for use in epidemiologic studies of the association between diet and disease. Review of the audiotapes of the interviews showed that most errors made in obtaining a dietary assessment were not detectable from visual review of the data. Although the quality-control procedures were developed for a computerized diet history questionnaire, they are applicable to other dietary assessment methods.

Adult↗
PubMed1993

Genetic basis of familial dyslipidemia and hypertension: 15-year results from Utah.

The genetic and environmental determinants of hypertension, lipid abnormalities, and coronary artery disease (CAD) have been studied for 15 years in Utah in population-based multigenerational pedigrees (2500 subjects among 98 pedigrees), twin pairs (74 monozygous and 78 dizygous), hypertensive siblings (131 sibships), siblings with CAD before age 55 (45 sibships), and anecdotally ascertained pedigrees with type II diabetes (271 subjects among 16 pedigrees), lipoprotein lipase deficiency (106 subjects in a single pedigree), and familial hypercholesterolemia (502 heterozygotes among 50 pedigrees). Estimates of heritability ranged from 20 to 75% for blood pressures and blood lipids. A strong positive family history predicts a future occurrence of hypertension (relative risk [RR] = 3.8) and CAD (RR = 12.7). Segregating single-gene effects were found for several 'intermediate phenotypes' associated with hypertension (erythrocyte sodium-lithium countertransport, intraerythrocytic sodium, a relative fat pattern, total urinary kallikrein excretion, and fasting insulin levels). Strong single-gene effects in segregation analysis were also found for low-density lipoprotein (LDL) cholesterol, lipoprotein (a) (Lp[a]), low high-density lipoprotein (HDL) cholesterol, and high apolipoprotein (apo) B. Deoxyribonucleic acid (DNA) markers of lipid abnormalities or hypertension have included LDL-receptor defects, lipoprotein lipase deficiency, high Lp(a), familial defective apo B, decreased quantitative levels of apo B, apo E phenotype, angiotensinogen, and 'glucocorticoid remediable aldosteronism (GRA) hypertension.' Also tested in Utah studies, but not found to be DNA markers for hypertension, were the genetic loci for the structural genes for renin and angiotensin-converting enzyme, and the sodium antiport system. In addition, important gene-gene interactions (LDL receptor with apo E2) and gene-environment interactions (kallikrein with potassium intake) were found.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1993

Is survival among women diagnosed with breast cancer influenced by family history of breast cancer?

In this study, we examine the association between having a family history of breast cancer and survival after diagnosis with breast cancer. Data for this study were from the Utah Population Database, a linked database consisting of genealogy data of Mormon pioneer families, Utah Cancer Registry data, and Vital Statistics data. We observed that women who had a mother with breast cancer were more likely to die of any cause than women without a mother with breast cancer [hazard rate ratio (HRR) = 1.36, 95% confidence limits (CL) = 1.04, 1.79], as were women with over 30 female relatives with breast cancer (HRR = 1.69, 95% CL = 1.16, 2.45). Similar findings were observed for women dying of breast cancer. Other indicators of family history were not associated with survival except within specific age groups. Women diagnosed with breast cancer at age 50 or before had poorer survival if they had a family history of breast cancer. Relative risk estimates were 1.54 (95% CL = 0.98, 2.41) for first degree relative, 1.55 (95% CL = 0.87, 2.78) for mother, and 2.65 (95% CL = 1.23, 5.74) for more than 30 female relatives with breast cancer.

Adult↗
PubMed1991

Genetic traits related to hypertension and electrolyte metabolism.

The genetic and cultural heritability and intercorrelation of traits related to hypertension have been carried out in 98 Utah pedigrees (2,500 person) and 58 sibships with two or more hypertensive persons (131 hypertensive persons). Although none of these traits has been established as a marker for "sodium-sensitive hypertension," many of them are related at least indirectly to both electrolyte metabolism and risk of hypertension. Significant recessive monogenic effects and high total heritability (52-84%) were found for urinary kallikrein, high fat pattern index, intraerythrocytic sodium, Na-Li countertransport, and ouabain binding sites. Familial correlations more strongly attributable to shared environment than to genetic effects were found for Na,K-ATPase pump activity, intraerythrocytic magnesium, plasma digoxin-like factor, plasma renin activity, and plasma sodium concentration. All anthropometric variables tested showed highly significant genetic heritability with low and insignificant shared family environmental effects. Several of the genetically determined cellular cation tests also correlated with other genetic traits including plasma lipids, anthropometric measurements, and other cellular cation tests. Among hypertensive individuals with familial dyslipidemic hypertension, plasma insulin levels correlated with obesity and lipid abnormalities and with several cellular cation flux tests associated with hypertension.

Adolescent↗
PubMed1991

Are there interactions and relations between genetic and environmental factors predisposing to high blood pressure?

An overview of published observations suggests that both genetic predisposition and environment work together to produce hypertension in most persons. High blood pressure before age 55 occurs 3.8 times more often among persons with a strong positive family history of high blood pressure. Much of the total variability in blood pressure in modern populations seems attributable to genetic factors. Estimates of the proportion of the variance attributable to all genetic factors (heritability [H2]) vary from 25% in pedigree studies to 65% in twin studies for sitting diastolic blood pressure. Several biochemical traits associated with high blood pressure are highly genetic (H2, 78-84%) and may help elucidate the pathophysiology of high blood pressure. While pertinent environmental factors such as salt intake, alcohol use, and amount of exercise also correlate significantly among relatives, only 7% of the total variance of diastolic blood pressure seems attributable to all shared environmental factors in family households. Thus most familial aggregation of high blood pressure appears to be due to genes rather than shared family environment. Practical benefit may result from identifying familial predisposition in multiple siblings with high blood pressure before age 55 and lipid abnormalities (labeled "familial dyslipidemic hypertension"). About 12% of high blood pressure patients have familial dyslipidemic hypertension and also have high risk of early coronary heart disease. Hyperinsulinemia and central obesity as well as high triglycerides and low high density lipoprotein cholesterol are prominent features of familial dyslipidemic hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcohol Drinking↗
PubMed1990

Genetics of hypertension: what we know and don't know.

Human arterial hypertension is likely a multifactorial trait resulting from multiple measurable monogenes, blended polygenes, shared family environment, and individual environment. Familial aggregation of hypertension and familial correlation of blood pressure appears to be more due to genes than to shared family environment. Total genetic heritability of 80% with some recessive major gene effects have been found for several traits associated with hypertension including urinary kallikrein excretion, intraerythrocytic sodium, and sodium-lithium countertransport. Other interesting factors regarding hypertension genetics include: non-modulation of the renin angiotensin system, intralymphocytic sodium, ionized calcium, and several genetic markers such as haptoglobin, HLA, and MNS blood type. Probably the most clinically useful information regarding the genetics of hypertension is evolving in several studies reporting a strong association of hypertension with dyslipidemia, diabetes, and obesity.

Environment↗
PubMed1990

Multigenic human hypertension: evidence for subtypes and hope for haplotypes.

Hypertension that occurs before the age of 60 years is strongly aggregated in families, mostly due to genetic factors with weaker contributions from a shared family environment. Hypertension is probably a heterogeneous collection of overlapping subsets of pathophysiological mechanisms, such as dyslipidemia, obesity, hyperinsulinemia and cation metabolism. Highly heritable traits such as sodium-lithium countertransport, urinary kallikrein excretion and a body fat pattern index show evidence of major gene segregation in families with hypertension. They are thought to be intermediate phenotypes in the chain of pathophysiological events leading from specific genes to the distant phenotype of hypertension. They provide evidence of measurable contributions from single gene traits to the susceptibility to hypertension. Genetic linkage studies have suggested that other specific loci (e.g. histocompatibility leukocyte antigen, blood group MN and the haptoglobin protein) contribute to the susceptibility to hypertension. DNA sequencing has shown a point mutation for lipoprotein lipase that conveys susceptibility to lipid abnormalities, and possibly also hypertension, as seen in families with dyslipidemic hypertension. Further application of these approaches, especially in families that include multiple siblings with hypertension, shows promise of a true understanding of how the combined effects of a few specific genes, the polygenic background and selected environmental factors can lead to essential hypertension. This understanding should foster better tailored and more effective approaches to the prevention, diagnosis and treatment of hypertension.

Blood Pressure↗
PubMed1989

Current knowledge regarding the genetics of human hypertension.

Observations over 11 years from the University of Utah Cardiovascular Genetics Research Clinic and published data from other studies are reviewed to illustrate research approaches, developing results and prospects for future studies. Strong associations with hypertension have been found for several biochemical tests that show substantial genetic determination. Suggestions of recessive major gene effects and significant polygenic background determinations have been found for several variables, including urinary kallikrein excretion, intracellular sodium concentration, sodium-lithium countertransport and sodium-potassium cotransport. Each of these variables is related in some way to sodium or potassium metabolism, or both, and may help to improve the understanding of a possibly inherited susceptibility to hypertension that is related to dietary electrolyte intake. A second major group of factors involving familial predisposition to hypertension include lipid abnormalities (increased very-low- and low-density lipoprotein cholesterol and decreased high-density lipoprotein cholesterol); increased fasting insulin levels or insulin resistance, or both; obesity (especially central or upper body obesity); and multiple environmental factors influencing these metabolic systems, including dietary fat, carbohydrate and calorie intake; physical exercise; and certain antihypertensive medications that adversely affect lipid metabolism and glucose tolerance. Some studies even suggest a possible link between these two large groups of factors (electrolyte metabolism and lipid-insulin metabolism). Hypertriglyceridaemia and hyperinsulinaemia are both significantly correlated with increased levels of several cation-flux tests. It is recommended that studies of human hypertension apply these biochemical profiles to study sibships with two or more hypertensive siblings as a cost-effective initial approach.(ABSTRACT TRUNCATED AT 250 WORDS)

Diabetes Mellitus↗
PubMed1989

A gene for high urinary kallikrein may protect against hypertension in Utah kindreds.

The inheritance of 12-hour overnight total urinary kallikrein excretion and its association with family history of essential hypertension were studied in 405 normotensive adults and 391 youths in 57 Utah pedigrees. Total urinary kallikrein excretion was highly familial with 51% of the total variance attributable to a dominant allele for high total urinary kallikrein excretion and 27% attributable to the combined effects of polygenes and shared family environment. An estimated 28% of the population has one or two copies of the dominant allele for high total urinary kallikrein excretion (2.3 SD units higher than the low homozygotes). About 83% of the population could be assigned to one of the two genotypic populations. Individuals with the high total urinary kallikrein excretion genotype were significantly less likely to have one or two hypertensive parents (relative odds = 0.56, p = 0.042). We conclude that a dominant allele expressed as high total urinary kallikrein excretion may be associated with decreased risk of essential hypertension. Further studies should be performed to confirm this finding and to test for interactions between this apparently protective gene and other genetic and environmental determinants of essential hypertension.

Adolescent↗
PubMed1988

Definition of genetic factors in hypertension: a search for major genes, polygenes, and homogeneous subtypes.

Essential hypertension is a heterogeneous group of disorders with different causes. This report reviews approaches taken and results found in current studies of the genetic and environmental determinants of essential hypertension. Recent observations from the University of Utah Cardiovascular Genetics Research Clinic and published data from other studies are cited. Several biochemical tests show strong associations with hypertension and substantial major gene and/or polygenic determination including: urinary kallikrein excretion, intracellular sodium concentration, sodium-lithium countertransport, plasma haptoglobin phenotypes, MN blood groups, and familial dyslipidemia.

Genes↗