Low-fat High-fiber Diet Research Articles

An Apple a Day Keeps the Doctor Away: The Effect of a Low-Fat, High-Fiber Diet on Quality of Life, Inflammation, and Dysbiosis in Patients With Ulcerative Colitis

An Apple a Day Keeps the Doctor Away: The Effect of a Low-Fat, High-Fiber Diet on Quality of Life, Inflammation, and Dysbiosis in Patients With Ulcerative Colitis

Low-Fat, High-Fiber Diet Reduces Markers of Inflammation and Dysbiosis and Improves Quality of Life in Patients With Ulcerative Colitis

A high-fat diet has been associated with an increased risk of ulcerative colitis (UC). We studied the effects of a low-fat, high-fiber diet (LFD) vs an improved standard American diet (iSAD, included higher quantities of fruits, vegetables, and fiber than a typical SAD). We collected data on quality of life, markers of inflammation, and fecal markers of intestinal dysbiosis in patients with UC. We analyzed data from a parallel-group, cross-over study of 17 patients with UC in remission or with mild disease (with a flare within the past 18 mo), from February 25, 2015, through September 11, 2018. Participants were assigned randomly to 2 groups and received a LFD (10% of calories from fat) or an iSAD (35%-40% of calories from fat) for the first 4-week period, followed by a 2-week washout period, and then switched to the other diet for 4 weeks. All diets were catered and delivered to patients' homes, and each participant served as her or his own control. Serum and stool samples were collected at baseline and week 4 of each diet and analyzed for markers of inflammation. We performed 16s ribosomal RNA sequencing and untargeted and targeted metabolomic analyses on stool samples. The primary outcome was quality of life, which was measured by the short inflammatory bowel disease (IBD) questionnaire at baseline and week 4 of the diets. Secondary outcomes included changes in the Short-Form 36 health survey, partial Mayo score, markers of inflammation, microbiome and metabolome analysis, and adherence to the diet. Participants' baseline diets were unhealthier than either study diet. All patients remained in remission throughout the study period. Compared with baseline, the iSAD and LFD each increased quality of life, based on the short IBD questionnaire and Short-Form 36 health survey scores (baseline short IBD questionnaire score, 4.98; iSAD, 5.55; LFD, 5.77; baseline vs iSAD, P= .02; baseline vs LFD, P= .001). Serum amyloid A decreased significantly from 7.99 mg/L at baseline to 4.50 mg/L after LFD (P= .02), but did not decrease significantly compared with iSAD (7.20 mg/L; iSAD vs LFD, P= .07). The serum level of C-reactive protein decreased numerically from 3.23 mg/L at baseline to 2.51 mg/L after LFD (P= .07). The relative abundance of Actinobacteria in fecal samples decreased from 13.69% at baseline to 7.82% after LFD (P= .017), whereas the relative abundance of Bacteroidetes increased from 14.6% at baseline to 24.02% on LFD (P= .015). The relative abundance of Faecalibacterium prausnitzii was higher after 4 weeks on the LFD (7.20%) compared with iSAD (5.37%; P= .04). Fecal levels of acetate (an anti-inflammatory metabolite) increased from a relative abundance of 40.37 at baseline to 42.52 on the iSAD and 53.98 on the LFD (baseline vs LFD, P= .05; iSAD vs LFD, P= .09). The fecal level of tryptophan decreased from a relative abundance of 1.33 at baseline to 1.08 on the iSAD (P= .43), but increased to a relative abundance of 2.27 on the LFD (baseline vs LFD, P= .04; iSAD vs LFD, P= .08); fecal levels of lauric acid decreased after LFD (baseline, 203.4; iSAD, 381.4; LFD, 29.91; baseline vs LFD, P= .04; iSAD vs LFD, P= .02). In a cross-over study of patients with UC in remission, we found that a catered LFD or iSAD were each well tolerated and increased quality of life. However, the LFD decreased markers of inflammation and reduced intestinal dysbiosis in fecal samples. Dietary interventions therefore might benefit patients with UC in remission. ClinicalTrials.gov no: NCT04147598.

Impact of a High-Fat or High-Fiber Diet on Intestinal Microbiota and Metabolic Markers in a Pig Model.

To further elaborate interactions between nutrition, gut microbiota and host health, an animal model to simulate changes in microbial composition and activity due to dietary changes similar to those in humans is needed. Therefore, the impact of two different diets on cecal and colonic microbial gene copies and metabolic activity, organ development and biochemical parameters in blood serum was investigated using a pig model. Four pigs were either fed a low-fat/high-fiber (LF), or a high-fat/low-fiber (HF) diet for seven weeks, with both diets being isocaloric. A hypotrophic effect of the HF diet on digestive organs could be observed compared to the LF diet (p < 0.05). Higher gene copy numbers of Bacteroides (p < 0.05) and Enterobacteriaceae (p < 0.001) were present in intestinal contents of HF pigs, bifidobacteria were more abundant in LF pigs (p < 0.05). Concentrations of acetate and butyrate were higher in LF pigs (p < 0.05). Glucose was higher in HF pigs, while glutamic pyruvic transaminase (GPT) showed higher concentrations upon feeding the LF diet (p < 0.001). However, C-reactive protein (CRP) decreased with time in LF pigs (p < 0.05). In part, these findings correspond to those in humans, and are in support of the concept of using the pig as human model.

Intestinal Microbiota and Microbial Metabolites Are Changed in a Pig Model Fed a High-Fat/Low-Fiber or a Low-Fat/High-Fiber Diet.

The intestinal microbiota and its metabolites appear to be an important factor for gastrointestinal function and health. However, research is still needed to further elaborate potential relationships between nutrition, gut microbiota and host’s health by means of a suitable animal model. The present study examined the effect of two different diets on microbial composition and activity by using the pig as a model for humans. Eight pigs were equally allotted to two treatments, either fed a low-fat/high-fiber (LF), or a high-fat/low-fiber (HF) diet for 7 weeks. Feces were sampled at day 7 of every experimental week. Diet effects on fecal microbiota were assessed using quantitative real-time PCR, DNA fingerprinting and metaproteomics. Furthermore, fecal short-chain fatty acid (SCFA) profiles and ammonia concentrations were determined. Gene copy numbers of lactobacilli, bifidobacteria (P<0.001) and Faecalibacterium prausnitzii (P<0.05) were higher in the LF pigs, while Enterobacteriaceae were more abundant in the HF pigs (P<0.001). Higher numbers of proteins affiliated to Enterobacteriaceae were also present in the HF samples. Proteins for polysaccharide breakdown did almost exclusively originate from Prevotellaceae. Total and individual fecal SCFA concentrations were higher for pigs of the LF treatment (P<0.05), whereas fecal ammonia concentrations did not differ between treatments (P>0.05). Results provide evidence that beginning from the start of the experiment, the LF diet stimulated beneficial bacteria and SCFA production, especially butyrate (P<0.05), while the HF diet fostered those bacterial groups which have been associated with a negative impact on health conditions. These findings correspond to results in humans and might strengthen the hypothesis that the response of the porcine gut microbiota to a specific dietary modulation is in support of using the pig as suitable animal model for humans to assess diet-gut-microbiota interactions.Data are available via ProteomeXchange with identifier PXD003447.

A randomized parallel-group dietary study for stages II–IV ovarian cancer survivors

ObjectiveFew studies have examined the dietary habits of ovarian cancer survivors. Therefore, we conducted a study to assess the feasibility and impact of two dietary interventions for ovarian cancer survivors. MethodsIn this randomized, parallel-group study, 51 women (mean age, 53years) diagnosed with stages II–IV ovarian cancer were recruited and randomly assigned to a low fat, high fiber (LFHF) diet or a modified National Cancer Institute diet supplemented with a soy-based beverage and encapsulated fruit and vegetable juice concentrates (FVJCs). Changes in clinical measures, serum carotenoid and tocopherol levels, dietary intake, anthropometry, and health-related quality of life (HRQOL) were assessed with paired t-tests. ResultsThe recruitment rate was 25%, and the retention rate was 75% at 6months. At baseline, 28% and 45% of women met guidelines for intake of fiber and of fruits and vegetables, respectively. After 6months, total serum carotenoid levels and α- and β-carotene concentrations were significantly increased in both groups (P<0.01); however, β-carotene concentrations were increased more in the FVJC group. Serum β-cryptoxanthin levels, fiber intake (+5.2g/day), and daily servings of juice (+0.9servings/day) and vegetables (+1.3servings/day) were all significantly increased in the LFHF group (all P<0.05). Serum levels of albumin, lutein and zeaxanthin, retinol, and retinyl palmitate were significantly increased in the FVJC group (all P<0.05). No changes in cancer antigen-125, anthropometry, or HRQOL were observed. ConclusionOverall, this study supports the feasibility of designing dietary interventions for stages II–IV ovarian cancer survivors and provides preliminary evidence that a low fat high fiber diet and a diet supplemented with encapsulated FVJC may increase phytonutrients in ovarian cancer survivors.

Effect of low-fat high-fiber diet and exercise program on hypertension and Metabolic Syndrome

Effect of low-fat high-fiber diet and exercise program on hypertension and Metabolic Syndrome

Low-Fat High-Fiber Diet Decreased Serum and Urine Androgens in Men

To validate our hypothesis that reduction in dietary fat may result in changes in androgen metabolism, 39 middle-aged, white, healthy men (50-60 yr of age) were studied while they were consuming their usual high-fat, low-fiber diet and after 8 wk modulation to an isocaloric low-fat, high-fiber diet. Mean body weight decreased by 1 kg, whereas total caloric intake, energy expenditure, and activity index were not changed. After diet modulation, mean serum testosterone (T) concentration fell (P < 0.0001), accompanied by small but significant decreases in serum free T (P = 0.0045), 5 alpha-dihydrotestosterone (P = 0.0053), and adrenal androgens (androstendione, P = 0.0135; dehydroepiandrosterone sulfate, P = 0.0011). Serum estradiol and SHBG showed smaller decreases. Parallel decreases in urinary excretion of some testicular and adrenal androgens were demonstrated. Metabolic clearance rates of T were not changed, and production rates for T showed a downward trend while on low-fat diet modulation. We conclude that reduction in dietary fat intake (and increase in fiber) results in 12% consistent lowering of circulating androgen levels without changing the clearance.

Coagulation and fibrinolysis abnormalities in obesity.

Abnormalities in coagulation and haemostasis represent a well-known link between obesity and thrombosis (both arterial and venous). Several studies have shown that obese patients have higher plasma concentrations of all pro-thrombotic factors (fibrinogen, vonWillebrand factor (vWF), and factor VII), as compared to non-obese controls, with a positive association with central fat. Similarly, plasma concentrations of plasminogen activator inhibitor-1 (PAI-1) have been shown to be higher in obese patients as compared to non-obese controls and to be directly correlated with visceral fat. Furthermore, obesity is characterized by higher plasma concentrations of anti-thrombotic factors, such as tissue-type plasminogen activator (t-PA) and protein C, as compared to non-obese controls, the increase in these factors being likely to represent a protective response partly counteracting the increase in pro-thrombotic factors. The issue of whether adipose tissue contributes directly to plasma PAI-1, its products stimulating other cells to produce PAI-1, or whether it primarily contributes indirectly has not yet been resolved. It has been proposed that the secretion of interleukin-6 (IL-6) by adipose tissue, combined with the actions of adipose tissue-expressed TNF-alpha in obesity, could underlie the association of insulin resistance with endothelial dysfunction, coagulopathy, and coronary heart disease. The role of leptin in impairing haemostasis and promoting thrombosis has been recently reported. Finally, some hormonal abnormalities (androgen, F, catecholamines) associated with the accumulation of body fat may contribute to the impairment of coagulative pathway in obesity. As to intervention strategies, dietary (i.e., low-fat high-fiber diet) and lifestyle (i.e., physical activity) measures have been demonstrated to be effective in improving the obesity-associated pro-thrombotic risk profile.

Pushing the envelope of nutrition support: complementary therapies

When the survey on unconventional medicine in the USA appeared in the New England Journal of Medicine in January 1993, most practitioners were surprised at the findings.1 One-third of those surveyed were using at least one unconventional therapy. However, in 1992, the National Institutes of Health (NIH) had already established an Office Alternative Medicine (OAM). An NIH workshop on alternative medicine was held in late 1992, from which a report on alternative medical systems and practices in the United States was later published.2 Six fields of alternative medicine were identified: 1. alternative systems of practice 2. bioelectromagnetic applications 3. diet/nutrition/lifestyle changes 4. herbal medicines 5. manual healing methods 6. mind/body control 7. pharmacologic and biological treatments The six NIH categories listed for diet, nutrition, and lifestyle changes were: 1. changes in lifestyle 2. diet 3. Gerson therapy 4. macrobiotics 5. megavitamins 6. nutrition supplements For clinical nutrition practitioners counseling patients on therapeutic diets, this report came as somewhat of a surprise. We did not consider that the low-fat–high-fiber diet, lots of fruits and vegetables, the vegetarian diet, or the Asian or Mediterraneanstyle diet regimens as being under the guise of complementary or alternative therapy. In addition, during the 1990s, growing interest in and use of optimal levels of individual vitamins, minerals, and phytochemicals by the lay public in general and cancer patients in particular thrust nutrition health professionals into this new area of practice. We found ourselves needing to be knowledgable and involved in this rapidly expanding field to provide responsible information and advice to patients and clients. The area of true concern for nutritionists and all health professionals is patient use of unproven nutrition regimens and diet therapies in place of traditional therapy and treatment for cancer. Alternative dietary management is usually combined into regimens referred to as “metabolic therapies.”3 These therapies are unproved, are not based on sound scientific principles, or have failed to show efficacy in studies or controlled clinical trials. Metabolic-therapy practitioners believe that most diseases, including cancer, result from an accumulation of toxins that must be removed from the body. This accumulation is the result of an unhealthy lifestyle; the consumption of unnatural foods; food preservatives and additives; the use of pesticides; and industrial pollution, which in turn lead to disruption of the immune system and susceptibility to degenerative diseases. However, when one looks at complementary and alternative medicine (CAM) dietary regimens, one sees a striking resemblance to current conventional dietary practices. Common features of CAM diets are: 1. usually plant based (vegetarian) 2. usually low in dietary fat and high in fiber 3. plenty of fruits and vegetables 4. most often result in weight loss These recommendations are similar to the dietary goals used by the American Heart Association, the American Cancer Society, the US Dietary Guidelines, and the American Dietetic Association. Obviously, practiced in the conventional setting as we present them, these are healthy eating patterns. In contrast, a number of CAM nutrition therapies appear questionable. The following are some of the better-known alternative nutrition regimens3,4: 1. Gerson therapy 2. Kelley regime 3. macrobiotic diet 4. Harold Manner diet 5. the Hoxsey regimen 6. the Livingston Wheeler regimen Another rapidly growing area of interest to patients is the use of herbal therapies or botanicals. Of the more than 1000 agents known, the following are popular choices, especially among cancer patients:5,6 1. astragalus 2. echinacea 3. cat’s claw 4. essiac 5. ginger 6. goldenseal 7. ginseng 8. garlic 9. iscador (mistletoe) 10. kombucha tea 11. laetrile 12. milk thistle (silymarin) 13. pau d’arco (lapachol) 14. pycnogenol 15. shiitake mushrooms When considering garlic, a common agent familiar to all of us, one can appreciate the difficulty in trying to become an expert on these products as herbal therapies. Research is available on many of these agents, but the studies are often conflicting, and study designs are not always well controlled. As noted, even this food product is not always benign if ingested in excessive amounts by patients with preexisting medical conditions.

Effect of highly purified eicosapentaenoic acid ethyl ester on insulin resistance and hypertension in Dahl salt-sensitive rats.

We investigated the effect of long-term administration of highly purified eicosapentaenoic acid ethyl ester (EPA-E), an n-3 polyunsaturated fatty acid derived from fish oil, in comparison to lard on the development of hypertension and insulin resistance in Dahl salt-sensitive (Dahl-S) rats fed a high-sucrose diet (HSD), a model of salt-sensitive hypertension. After 16 weeks of treatment, the glucose infusion rate (GIR) during the euglycemic insulin-glucose clamp test significantly increased in the HSD-EPA-E group compared with the HSD-water or -lard control group. The GIR was approximately three times higher in the HSD-EPA-E group versus the HSD-water or -lard control group, and it was about 70% of the rate in the calorically deprived control group fed a low-fat-high-fiber diet (LF-HFD). In addition, EPA-E significantly suppressed the elevation of plasma glucose and insulin levels after oral glucose loading. These results indicate that EPA-E prevents the development of insulin resistance in Dahl-S rats fed a HSD. Fatty acid analysis of phospholipids in skeletal muscle showed a significant increase in C18:2, C20:5, and C22:5 components in the HSD-EPA-E group and, conversely, a significant decrease in C16:0, C20:4, and C22:6. The present results indicate that the beneficial effect of EPA-E on insulin resistance in Dahl-S rats fed a HSD is likely dependent on the modification of phospholipid components in the skeletal muscle membrane. These findings suggest that EPA-E might prevent the development of insulin resistance in dietary obesity. In addition, the HSD-EPA-E group showed a significant increase in the level of uncoupling protein (UCP) in brown adipose tissue as compared with the HSD-water or -lard control group. However, EPA-E had no effect on the development of hypertension and obesity in Dahl-S rats fed the HSD.

Effects of lowering fat and increasing dietary fiber on fasting and postprandial plasma lipids in hypercholesterolemic subjects consuming a mixed Mediterranean-Western diet

The aim of this study was to evaluate the cholesterol-lowering effects of reducing fat and increasing or not increasing dietary fiber in subjects consuming a mixed Mediterranean-Western diet. Thirty-one free-living, mildly hypercholesterolemic subjects were randomly allocated to two groups. Subjects in both groups first shifted for 4 wk to a low-fat, low-fiber diet (LFLFD). For an additional 4-wk period, subjects in group 1 continued consuming the LFLFD whereas subjects in group 2 consumed a low-fat, high-fiber diet (LFHFD). Most dietary fatty acids were monounsaturated (38-41%) and fibers, when provided (up to 35 g/d), came from unrefined cereals, legumes, and soluble-fiber-enriched ready-to-eat cereals. After period 1 of the LFLFD, mean serum and low-density-lipoprotein (LDL)-cholesterol concentrations of subjects in groups 1 (-12.5% and -15.5%, respectively) and 2 (-10.5% and -15.5%, respectively) decreased significantly from baseline (P < 0.05). After period 2, mean serum and LDL-cholesterol concentrations of subjects consuming the LFLFD (group 1) were still lower (by 8.8% and 9.2%, respectively, from baseline) whereas in subjects consuming the LFHFD (group 2) these values decreased further to significantly lower values (14.2% and 17.6% from baseline, respectively). Fasting high-density-lipoprotein (HDL) cholesterol, apolipoprotein A-I, glycemia, and insulinemia did not change significantly. In seven men, postprandial lipemia transiently increased more after a breakfast test meal at the completion of the LFHFD period than after the LFLFD period. In conclusion, an LFHFD more comparable with the traditional Mediterranean diet may improve the dietary management of moderate hypercholesterolemia.

Genetic epidemiology and the future of disease prevention and public health.

As he chats with the young mother, the doctor flicks a cotton swab into the mouth of her infant son, collecting a small sample of mucus from inside his cheek. In the back room of his office, he inserts the sample into a machine, which extracts DNA from the mucus cells and compares it with the genetic material on a dime-size chip. Minutes later, a computer printer begins to spit out a list of the infant's genes. Fortunately, all but a few genes are labeled 'normal.' It is those few that the doctor discusses as he explains the results to the mother. 'Your son's genetic inheritance is generally good', he says 'but he is somewhat predisposed to skin lesions. So starting right away, he should be protected against excessive exposure to the sun.' And the doctor warns, 'he may well be susceptible to cardiovascular disease later in life. To lessen this risk, after about age 2, he should begin a lifelong low-fat high fiber diet' (1, p. 24).

Effect of high‐fat and low‐fiber meals on the cell proliferation activity of colorectal mucosa

Normal healthy volunteers (n = 43) were divided into four groups that received diets providing low or high levels of dietary fat (33 or 96 g/day) and low or high levels of dietary fiber (6 and 41 g/day) for a period of five days. Proliferation was assessed with tritiated thymidine labeling of three rectal biopsies. After five days on the prescribed diets, the average thymidine labeling index (LI) of the group on the high fat-low fiber diet was only 25% higher than the average LI of the group on the low fat-high fiber diet, a difference that is not statistically significant. We conclude that a short-term increase in dietary fat and decrease in dietary fiber does not result in a large increase in cell proliferation rate.

Estrogens, breast cancer, and intestinal flora.

Epidemiologic evidence has linked diet to breast cancer, with the highest cancer rates observed in women who eat a high fat-low fiber diet. There is also substantial information, both clinical and experimental, that implicates estrogens in the etiology of breast cancer. A recent study from our laboratory has shown that diet influences levels of estrogens, and the main mechanism is metabolism of estrogens in the intestine. The intestinal microflora plays a key role in the enterohepatic circulation of estrogens by deconjugating bound estrogens that appear in the bile, thereby permitting the free hormones to be reabsorbed. By suppressing the microflora with antibiotic therapy, fecal estrogens increase and urinary estrogens decrease, changes indicating diminished intestinal reabsorption. A low fat-high fiber diet is associated with similar findings-high fecal estrogens and low urinary estrogens. It appears that the microflora plays a key role in the metabolism of female sex hormones.