Answer: Try eating more probiotic-rich yogurt and other fermented foods rich in probiotics or taking probiotic supplements to increase your gut diversity.
It doesn’t sound healthy that overweight people have a much smaller range of gut flora than lean people do. Yogurt is rich in probiotic flora.
Dairy augmentation of total and central fat loss in obese subjects.
Abstract
BACKGROUND AND OBJECTIVE:
We have previously demonstrated an antiobesity effect of dietary Ca; this is largely mediated by Ca suppression of calcitriol levels, resulting in reduced adipocyte intracellular Ca2+ and, consequently, a coordinated increase in lipid utilization and decrease in lipogenesis. Notably, dairy Ca is markedly more effective than other Ca sources.
DESIGN:
Obese subjects were placed on balanced deficit (-500 kcal/day) diets and randomized to control (400-500 mg Ca/day; n = 16) or yogurt (1100 mg Ca/day; n = 18) treatments for 12 weeks. Dietary macronutrients and fiber were held constant at the US average.
MEASUREMENTS:
Body weight, body fat and fat distribution (by dual-energy X-ray absorptiometry), blood pressure and circulating lipids were measured at baseline and after 12 weeks of intervention.
RESULTS:
Fat loss was markedly increased on the yogurt diet (-4.43+/-0.47 vs -2.75+/-0.73 kg in yogurt and control groups; P<0.005) while lean tissue loss was reduced by 31% on the yogurt diet. Trunk fat loss was augmented by 81% on the yogurt vs control diet (P<0.001), and this was reflected in a markedly greater reduction in waist circumference (-3.99+/-0.48 vs -0.58+/-1.04 cm, P<0.001). Further, the fraction of fat lost from the trunk was higher on the yogurt diet vs control (P<0.005).
CONCLUSION:
Isocaloric substitution of yogurt for other foods significantly augments fat loss and reduces central adiposity during energy restriction..
The microbiome and obesity: is obesity linked to our gut flora?
Abstract
The human gut is a lush microbial ecosystem containing about 100 trillion microorganisms, whose collective genome, the microbiome, contains 100-fold more genes than the entire human genome. The symbiosis of our extended genome plays a role in host homeostasis and energy extraction from diet. In this article, we summarize some of the studies that have advanced the understanding of the microbiome and its effects on metabolism, obesity, and health. Metagenomic studies demonstrated that certain mixes of gut microbiota may protect or predispose the host to obesity. Furthermore, microbiota transplantation studies in germ-free murine models showed that the efficient energy extraction traits of obese-type gut flora are transmissible. The proposed methods by which the microbiome may contribute to obesity include increasing dietary energy harvest, promoting fat deposition, and triggering systemic inflammation. Future treatments for obesity may involve modulation of gut microbiota using probiotics or prebiotics.
And this study:
A core gut microbiome in obese and lean twins.
Abstract
The human distal gut harbours a vast ensemble of microbes (the microbiota) that provide important metabolic capabilities, including the ability to extract energy from otherwise indigestible dietary polysaccharides. Studies of a few unrelated, healthy adults have revealed substantial diversity in their gut communities, as measured by sequencing 16S rRNA genes, yet how this diversity relates to function and to the rest of the genes in the collective genomes of the microbiota (the gut microbiome) remains obscure. Studies of lean and obese mice suggest that the gut microbiota affects energy balance by influencing the efficiency of calorie harvest from the diet, and how this harvested energy is used and stored. Here we characterize the faecal microbial communities of adult female monozygotic and dizygotic twin pairs concordant for leanness or obesity, and their mothers, to address how host genotype, environmental exposure and host adiposity influence the gut microbiome. Analysis of 154 individuals yielded 9,920 near full-length and 1,937,461 partial bacterial 16S rRNA sequences, plus 2.14 gigabases from their microbiomes. The results reveal that the human gut microbiome is shared among family members, but that each person’s gut microbial community varies in the specific bacterial lineages present, with a comparable degree of co-variation between adult monozygotic and dizygotic twin pairs. However, there was a wide array of shared microbial genes among sampled individuals, comprising an extensive, identifiable ‘core microbiome’ at the gene, rather than at the organismal lineage, level. Obesity is associated with phylum-level changes in the microbiota, reduced bacterial diversity and altered representation of bacterial genes and metabolic pathways. These results demonstrate that a diversity of organismal assemblages can nonetheless yield a core microbiome at a functional level, and that deviations from this core are associated with different physiological states (obese compared with lean).
Read the complete scientific paper:
A core gut microbiome in obese and lean twins
Interesting mouse study:
Obesity, metabolic syndrome, and microbiota: multiple interactions.
Abstract
The incredible number and diversity of microorganisms in the human gastrointestinal tract represent a very diverse set of features, which support the host in important functions such as digestion of complex carbohydrates. Conventionalization of germ-free mice with a normal gut microbiota harvested from the intestine of conventionally raised mice results in weight gain and obesity. Development of obesity in genetically or diet-induced obese mice is associated with dramatic changes in the composition and metabolic function of the microbiota. This trait is transmissible as colonization of germ-free mice with an “obese-gut-derived” microflora results in a much greater increase in total body fat and leads to obesity. The first studies in obese and lean twins suggest that a core gut microbiome exists, and that obese individuals exhibit reduced diversity and an altered representation of metabolic pathways in their microbiota. Diet may have a fundamental effect on the composition of our microbiota. Early studies highlight the importance for specific diets such as a high-fat diet, which efficiently and very rapidly (within a single day) modulates the gut microbiome. The innate immune system might influence the metabolic syndrome and obesity, as mice deficient in Toll-like receptor 5 develop hyperphagia, become obese and insulin resistant. Importantly, transmission of the microbiota from these mice to healthy mice results in features of the metabolic syndrome. Available data suggest that the microbiota might play a role in the development of metabolic syndrome and obesity.
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This prospective observational study found that eating yogurt was the food associated with the most weight loss over time in a sample of over 120,000 people. Maybe there is something magical about yogurt and the probiotics it contains:
Changes in diet and lifestyle and long-term weight gain in women and men.
Abstract
BACKGROUND:
Specific dietary and other lifestyle behaviors may affect the success of the straightforward-sounding strategy “eat less and exercise more” for preventing long-term weight gain.
METHODS:
We performed prospective investigations involving three separate cohorts that included 120,877 U.S. women and men who were free of chronic diseases and not obese at baseline, with follow-up periods from 1986 to 2006, 1991 to 2003, and 1986 to 2006. The relationships between changes in lifestyle factors and weight change were evaluated at 4-year intervals, with multivariable adjustments made for age, baseline body-mass index for each period, and all lifestyle factors simultaneously. Cohort-specific and sex-specific results were similar and were pooled with the use of an inverse-variance-weighted meta-analysis.
RESULTS:
Within each 4-year period, participants gained an average of 3.35 lb (5th to 95th percentile, -4.1 to 12.4). On the basis of increased daily servings of individual dietary components, 4-year weight change was most strongly associated with the intake of potato chips (1.69 lb), potatoes (1.28 lb), sugar-sweetened beverages (1.00 lb), unprocessed red meats (0.95 lb), and processed meats (0.93 lb) and was inversely associated with the intake of vegetables (-0.22 lb), whole grains (-0.37 lb), fruits (-0.49 lb), nuts (-0.57 lb), and yogurt (-0.82 lb) (P≤0.005 for each comparison). Aggregate dietary changes were associated with substantial differences in weight change (3.93 lb across quintiles of dietary change). Other lifestyle factors were also independently associated with weight change (P<0.001), including physical activity (-1.76 lb across quintiles); alcohol use (0.41 lb per drink per day), smoking (new quitters, 5.17 lb; former smokers, 0.14 lb), sleep (more weight gain with <6 or >8 hours of sleep), and television watching (0.31 lb per hour per day).
CONCLUSIONS:
Specific dietary and lifestyle factors are independently associated with long-term weight gain, with a substantial aggregate effect and implications for strategies to prevent obesity. (Funded by the National Institutes of Health and others.).
Read the complete scientific paper:
Changes in diet and lifestyle and long-term weight gain in women and men.
This study tested the probiotic supplementation idea in obese mice–but couldn’t show that their probiotics caused their mice to lose weight:
Effect of Lactobacillus acidophilus NCDC 13 supplementation on the progression of obesity in diet-induced obese mice.
Abstract
There is an increased interest in investigating the relationship between the gut microbiota and energy homeostasis. Probiotics are health beneficial microbes mainly categorised under the genus Lactobacillus and Bifidobacterium, which when administered in adequate amounts confer health benefits to the host, and have been implicated in various physiological functions. The potential role of probiotics in energy homeostasis is a current and an emerging area of research. In the present study, Lactobacillus acidophilus NCDC 13 was used to evaluate its anti-obesity potential in diet-induced obese (C57BL/6) mice. The probiotic bacterial culture was administered in Indian yogurt preparation called ‘dahi’, prepared using native starter cultures, and compared with control dahi containing only dahi starter cultures. The dietary intervention was followed for 8 weeks, and whole-body fat composition, and liver and muscle adiposity were measured using MRI. Changes in gut microbiota were assessed by fluorescent in situ hybridisation in faeces and caecal contents. The feeding of the probiotic brought no changes in body-weight gain, food and dahi intake when compared with the control dahi-fed animals. No significant changes in body fat composition, liver and muscle adiposity were also observed. At the end of the dietary intervention, a significant increase (P < 0·05) in the number of total Bifidobacterium was observed in both faeces and caecal contents of mice as a result of probiotic dahi administration. Thus, L. acidophilus NCDC 13 supplementation could be beneficial in shifting the gut microbiota balance positively. However, its anti-obesity potential could not be established in the present study and warrants further exploration.
But this earlier study showed that probiotics could delay onset of diabetes in rats:
Antidiabetic effect of probiotic dahi containing Lactobacillus acidophilus and Lactobacillus casei in high fructose fed rats.
Abstract
OBJECTIVE:
We investigated the effect of low-fat (2.5%) dahi containing probiotic Lactobacillus acidophilus and Lactobacillus casei on progression of high fructose-induced type 2 diabetes in rats.
METHODS:
Diabetes was induced in male albino Wistar rats by feeding 21% fructose in water. The body weight, food and water intakes, fasting blood glucose, glycosylated hemoglobin, oral glucose tolerance test, plasma insulin, liver glycogen content, and blood lipid profile were recorded. The oxidative status in terms of thiobarbituric acid-reactive substances and reduced glutathione contents in liver and pancreatic tissues were also measured.
RESULTS:
Values for blood glucose, glycosylated hemoglobin, glucose intolerance, plasma insulin, liver glycogen, plasma total cholesterol, triacylglycerol, low-density lipoprotein cholesterol, very low-density lipoprotein cholesterol, and blood free fatty acids were increased significantly after 8 wk of high fructose feeding; however, the dahi-supplemented diet restricted the elevation of these parameters in comparison with the high fructose-fed control group. In contrast, high-density lipoprotein cholesterol decreased slightly and was retained in the dahi-fed group. The dahi-fed group also exhibited lower values of thiobarbituric acid-reactive substances and higher values of reduced glutathione in liver and pancreatic tissues compared with the high fructose-fed control group.
CONCLUSION:
The probiotic dahi-supplemented diet significantly delayed the onset of glucose intolerance, hyperglycemia, hyperinsulinemia, dyslipidemia, and oxidative stress in high fructose-induced diabetic rats, indicating a lower risk of diabetes and its complications.
The effect of probiotic dahi containing Lactobacillus acidophilus and Lactobacillus casei on gastropathic consequences in diabetic rats.
Abstract
In the present study, the effects of oral administration of probiotic dahi containing Lactobacillus acidophilus and Lactobacillus casei on gastropathic consequences in streptozotocin-induced diabetic rats were evaluated, and effects were compared with skim milk- and control dahi-fed groups. The feeding of probiotic dahi did not change the blood glucose levels in chronic hyperglycemic conditions. The rate of charcoal transit was significantly higher in probiotic dahi-fed animals than in those of the diabetic control group (P < .05). Moreover, the oral administration of probiotic dahi significantly increased counts of lactobacilli adherent to epithelial walls and free in the lumen of the small and large intestine, while decreasing attached as well as free coliform counts (P < .05). In addition, probiotic dahi reversed the decrease in total lactobacilli and increase in total coliforms in fecal samples of diabetic animals. It was also shown that oral ingestion of probiotic dahi reduced the oxidative stress marker thiobarbituric acid-reactive species in intestinal tissues and glycosylation of hemoglobin (P < .05). All the effects were predominantly higher in the probiotic dahi-fed group than the skim milk- and control dahi-fed groups. The results indicate that probiotic dahi may be used as a therapeutic regimen to diminish the gastropathic consequences of diabetes.
Oral administration of dahi containing probiotic Lactobacillus acidophilus and Lactobacillus casei delayed the progression of streptozotocin-induced diabetes in rats.
Abstract
In this study, the effect of dahi containing probiotic Lactobacillus acidophilus NCDC14 and Lactobacillus casei NCDC19 (73 x 10(8) cfu/g) on progression of streptozotocin (STZ)-induced diabetes in rats (15 g/day/rat) for 28 days was investigated. Feeding of probiotic dahi significantly suppressed the incremental peaks and area under the curve and delayed reduction of insulin secretion during oral glucose tolerance test more than skim milk or control dahi. The feeding of milk products reduced the total cholesterol, triglycerides, LDL and VLDL-cholesterol and increased HDL-cholesterol levels (P<0.05). Moreover, probiotic dahi significantly suppressed STZ-induced oxidative damage in pancreatic tissues by inhibiting the lipid peroxidation and formation of nitric oxide, and preserving antioxidant pool such as glutathione content and activities of superoxide dismutase, catalase and glutathione peroxidase. The results suggest that the supplementation of probiotic Lb. acidophilus and Lb. casei with dahi cultures increased the efficacy of dahi to suppress STZ-induced diabetes in rats by inhibiting depletion of insulin as well as preserving diabetic dyslipidemia, and inhibiting lipid peroxidation and nitrite formation. This may empower antioxidant system of beta-cells and may slow down the reduction of insulin and elevation of blood glucose levels.
Probiotics in yogurt seem to be good for managing fasting glucose in Type 2 diabetes better, but had no effect on insulin levels:
Probiotic yogurt improves antioxidant status in type 2 diabetic patients.
Abstract
OBJECTIVE:
Oxidative stress plays a major role in the pathogenesis and progression of diabetes. Among various functional foods with an antioxidant effect, probiotic foods have been reported to repress oxidative stress. The objective of this clinical trial was to assess the effects of probiotic and conventional yogurt on blood glucose and antioxidant status in type 2 diabetic patients.
METHODS:
Sixty-four patients with type 2 diabetes mellitus, 30 to 60 y old, were assigned to two groups in this randomized, double-blind, controlled clinical trial. The patients in the intervention group consumed 300 g/d of probiotic yogurt containing Lactobacillus acidophilus La5 and Bifidobacterium lactis Bb12 and those in the control group consumed 300 g/d of conventional yogurt for 6 wk. Fasting blood samples, 24-h dietary recalls, and anthropometric measurements were collected at the baseline and at the end of the trial.
RESULTS:
Probiotic yogurt significantly decreased fasting blood glucose (P < 0.01) and hemoglobin A1c (P < 0.05) and increased erythrocyte superoxide dismutase and glutathione peroxidase activities and total antioxidant status (P < 0.05) compared with the control group. In addition, the serum malondialdehyde concentration significantly decreased compared with the baseline value in both groups (P < 0.05). No significant changes from baseline were shown in insulin concentration and erythrocyte catalase activity within either group (P > 0.05).
CONCLUSION:
The consumption of probiotic yogurt improved fasting blood glucose and antioxidant status in type 2 diabetic patients. These results suggest that probiotic yogurt is a promising agent for diabetes management.
Yogurt improved lipid function:
The effects of probiotic and conventional yoghurt on lipid profile in women.
Abstract
Many studies have been done on the hypocholesterolaemic effect of probiotic yoghurt. The results, however, are not conclusive. The aim of the present study was to test the effect of probiotic and conventional yoghurt on the lipid profile in women. In a randomised trial, ninety female volunteers aged 19-49 years were assigned to three groups. Subjects consumed daily 300 g probiotic yoghurt containing Lactobacillus acidophilus La5 and Bifidobacterium lactis Bb12 or 300 g conventional yoghurt or no yoghurt for 6 weeks. Fasting blood samples, 3 d dietary records and anthropometric measurements were collected at baseline (T1), end of week 3 (T2) and end of week 6 (T3). Lipid profile parameters were determined by enzymic methods. Results showed no significant difference in lipid profile within any group throughout the study. Comparing mean differences (T1 – T3) among the three groups showed: no difference in TAG and LDL-cholesterol, a decrease in cholesterol in both conventional (P < 0.05) and probiotic yoghurt groups (P < 0.005) compared with the control group, a decrease in total:HDL-cholesterol ratio for conventional (P < 0.05) and probiotic yoghurt groups (P < 0.001) compared with the control group, and an increase in HDL-cholesterol in the probiotic yoghurt group (P < 0.05) compared with the control group. Positive changes in lipid profile were observed in both yoghurt groups. Any added effect, therefore, is due to the consumption of fermented milk products.
Long-term consumption of fermented dairy products over 6 months increases HDL cholesterol.
Abstract
OBJECTIVE:
Assessment of the hypocholesterolaemic effect of yoghurt supplemented with Lactobacillus acidophilus 145 and Bifidobacterium longum 913 in women.
DESIGN:
The cross-over study consisted of three periods (7 weeks each): first period, control yoghurt for all 29 women; second period, probiotic yoghurt for 18 women, control yoghurt for 11 women; third period, the reverse of that in the second period.
SETTING:
Department of Nutritional Physiology, Institute of Nutritional Science, Friedrich Schiller University, Jena.
SUBJECTS:
Twenty-nine healthy women, aged 19-56 y. Fifteen of these were normocholesterolaemic and 14 women were hypercholesterolaemic.
INTERVENTION:
Yoghurt (300 g) daily containing 3.5% fat and starter cultures of Streptococcus thermophilus and L. lactis. Probiotic yoghurt was the control yoghurt enriched with L. acidophilus 145, B. longum 913 and 1% oligofructose (synbiotic).
RESULTS:
The mean serum concentration of total cholesterol and the LDL cholesterol was not influenced by the synbiotic (P>0.05). The HDL concentration increased significantly by 0.3 mmol/l (P=0.002). The ratio of LDL/HDL cholesterol decreased from 3.24 to 2.48 (P=0.001).
CONCLUSIONS:
The long-term daily consumption of 300 g yoghurt over a period of 21 weeks (control and synbiotic) increased the serum concentration of HDL cholesterol and lead to the desired improvement of the LDL/HDL cholesterol ratio.
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The gut microbiome as therapeutic target.
Source
Université Catholique de Louvain, Louvain Drug Research Institute, Metabolism and Nutrition Research Group, Brussels, Belgium. patrice.cani@uclouvain.be
Abstract
Obesity, type-2 diabetes and low-grade inflammation are becoming worldwide epidemics. In this regard, the literature provides a novel concept that we call “MicrObesity” (Microbes and Obesity), which is devoted to deciphering the specific role of dysbiosis and its impact on host metabolism and energy storage. In the present review, we discuss novel findings that may partly explain how the microbial community participates in the development of the fat mass development, insulin resistance and low-grade inflammation that characterise obesity. In recent years, numerous mechanisms have been proposed and several proteins identified. Amongst the key players involved in the control of fat mass development, Fasting induced adipose factor, AMP-activated protein kinase, G-protein coupled receptor 41 and G-protein coupled receptor 43 have been linked to gut microbiota. In addition, the discovery that low-grade inflammation might be directly linked to the gut microbiota through metabolic endotoxaemia (elevated plasma lipopolysaccharide levels) has led to the identification of novel mechanisms involved in the control of the gut barrier. Amongst these, the impacts of glucagon-like peptide-2, the endocannabinoid system and specific bacteria (e.g., Bifidobacterium spp.) have been investigated. Moreover, the advent of probiotic and prebiotic treatments appears to be a promising “pharmaco-nutritional” approach to reversing the host metabolic alterations linked to the dysbiosis observed in obesity. Although novel powerful molecular system biology approaches have offered great insight into this “small world within”, more studies are needed to unravel how specific changes in the gut microbial community might affect or counteract the development of obesity and related disorders.
Unraveling how probiotic yogurt works.
Source
Lawson Health Research Institute, and Department of Microbiology and Immunology, The University of Western Ontario, London, Ontario N6A 4V2, Canada.
Abstract
No matter what the advertisements are, or are not, allowed to say, it would be good to know if probiotic yogurt, in addition to its nutritional value, has a beneficial effect on the gut. In this issue, McNulty, Gordon and their colleagues describe a parallel series of human and animal studies designed to uncover the effects of probiotic yogurt on the gut microbiota. The intake of yogurt supplemented with five bacterial species, including the probiotic Bifidobacterium animalis, did not appreciably alter the composition of the human or mouse gut microbiota, but it did induce transcriptional and metabolic changes that reflected host bacterial responses to the arrival of the new species. This elegant study provides a strategy to delineate the precise effects exerted by probiotic foods on the human gut.
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A bit more support for an association between yogurt consumption and reduced risk of diabetes in postmenopausal women:
A diet high in low-fat dairy products lowers diabetes risk in postmenopausal women.
Abstract
Some previous studies have suggested that consuming dairy products, particularly the low-fat variety, lowers the incidence of type 2 diabetes. However, no study to our knowledge has focused on an ethnically diverse group of postmenopausal women, a population with a high risk of this disease. We conducted a prospective cohort study of 82,076 postmenopausal women enrolled in the Women’s Health Initiative Observational Study who did not report diabetes at enrollment. Total, low-fat, and high-fat dairy product and yogurt intakes were estimated from FFQ at baseline and 3 y of follow-up. Treated diabetes incidence was ascertained from annual follow-up questionnaires. During 8 y of follow-up, 3946 cases of incident treated diabetes were reported (annual incidence, 0.73%; cumulative incidence, 4.8%). After multivariable adjustment, low-fat dairy product consumption was inversely associated with the risk of type 2 diabetes. RR was roughly 0.5-0.6 in the upper quintiles compared with the lowest quintile (median servings/d, 2.8 in the 5th quintile and 1.5 in the 4th quintile vs. 0.05 in the first quintile; P-trend < 0.001). The inverse relationship was more pronounced in women with a higher BMI. High yogurt consumption was associated with a significant decrease in diabetes risk, whereas there was no relationship between high-fat dairy product consumption and diabetes risk. A diet high in low-fat dairy products is associated with lower diabetes risk in postmenopausal women, particularly those who are obese.
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