Stig Bengmark

Choose right carbohydrates and right fats (RCRF) - keys to optimal health

The main objective of this study was to investigate the effects of Synbiotic2000™ Forte on the intestinal motility and interstitial cells of Cajal (ICC) in traumatic brain injury (TBI) mouse model. Kunming mice were randomly divided into sham operation group (S group), enteral nutrition group with TBI (E group), and Synbiotic2000™ Forte group with TBI (P group). The contractile activity of the intestinal smooth muscle, densities and ultrastructure of the ICC, kit protein concentration, weight, and defecation of mice were monitored and analyzed. TBI markedly suppressed contractile activity of the intestinal smooth muscle (P < 0.01), which led to a reduction of defecation (P < 0.01) and weight (P < 0.01). However, application of Synbiotic2000™ Forte significantly improved contractile activity of the small intestine (P < 0.01), which may be related to protective effects to the interstitial cells of Cajal, smooth muscle cells, and enteric neurons. TBI impaired ICC networks and densities (P < 0.01), events that were protected by the application of Synbiotic2000™ Forte. Synbiotic2000™ Forte may attenuate TBI-mediated inhibition of the kit protein pathway. Synbiotic2000™ Forte may improve intestinal motility and protect the ICC in the TBI mouse. These findings provide a novel support for the application of Synbiotic2000™ Forte in intestinal motility disturbance after TBI.

Obesity, the deadly quartet and the contribution of the neglected daily organ rest - a new dimension of un-health and its prevention

Modern Western food contains less than twenty per cent of the ingredients on which our paleolithic ancestors lived and other primates like the wild chimpanzees live today. Fresh greens, fruits, seeds, piths, bark and insects were the foods to which humans had been adapted during millions of years. A recent study found that 80% of diet of wild chimpanzee consists of ripe and unripe fruits, young leaves, flowers and fresh and dry seeds, and roots/tubers used only in times of draft. In contrast Western food consists of more than fifty per cent refined carbohydrates (cooked, rice heated to very high temperatures, bread, pasta, potato and other tubers) and in another 25-30 per cent animal products and refined oils, leaving less than 20 per cent of their foods similar to those of our ancestors. The situation is even worse in critically ill patient, whose nutrition usually contains no greens at all. It is fully documented that these Western foods, when consumed in larger quantities are detrimental to health: inducing increased systemic inflammation; increased supply of and stimulation of IGF1, stimulation of Toll-like receptors, leading to obesity and an epidemic of chronic diseases, which has increased and continue to increase dramatically. Modern molecular biology techniques have made it possible to explore the mechanisms behind these catastrophic effects of modern living. It is a 50-year-old observation that beneficial bacteria like lactobacilli do not grow well when exposed to food ingredients such casein (dairy) and gluten (wheat, rye and barley). More recent Studies demonstrate that human microbiota and its functions compared to rural minorities, are more than 90 % reduced in Western individuals, and further reduced by exposure to chemicals, including pharmaceuticals. The ultimate consequence of these changes is that body membranes lose their tightness and start leaking; such leakage often documented for all body membranes; effects observed in barriers such as in the gut, airways, skin, oral cavity, vagina, nose, eye cavity, placenta and blood-brain barrier. The consequence of this is leakage over the membranes of various damaging toxins of microbial origin such as endotoxins, but also food-derived proteotoxins such as casein, gluten and zein and toxins producing by heating foods to high temperature (grilling, roasting, baking etc) and production of glycated and lipoxidated molecules (AGEs and ALEs). Furthermore, bacterial debris and whole dead or live bacteria will leak and found in the fat of obese and the plaques of individuals with arteriosclerosis. Recent studies report not only reduced numbers and diversity of bacteria in microbiota of individuals with various diseases, but also totally different microbial species in individuals with obesity and various diseases. Attempts to treat diseases by supplying probiotics have only been partly, and at the best temporarily, successful, when applied without any changes in food habits. Furthermore, probiotics are not compatible with pharmacological and other toxic chemicals. Eco-biological treatments, with plant-derived substances, or phytochemicals, e.g. curcumin and resveratrol, and pre-, pro- and synbiotics offer similar effects as use of drugs referred to asbiologicals, although milder but also without adverse effects. Such treatments should be tried as alternative therapies; mainly, to begin with, for disease prevention but also in early cases of chronic diseases. Dramatic alterations, in direction of a paleolithic-like lifestyle and food habits, appear, as we see it today, the only alternative to control the present escalating global health crisis.

Health care-induced diseases constitute a fast-increasing problem. Just one type of these health care-associated infections (HCAI) constitutes the fourth leading cause of death in Western countries. About 25 million individuals worldwide are estimated each year to undergo major surgery, of which approximately 3 million will never return home from the hospital. Furthermore, the quality of life is reported to be significantly impaired for the rest of the lives of those who, during their hospital stay, suffered life-threatening infections/sepsis. Severe infections are strongly associated with a high degree of systemic inflammation in the body, and intimately associated with significantly reduced and malfunctioning GI microbiota, a condition called dysbiosis. Deranged composition and function of the gastrointestinal microbiota, occurring from the mouth to the anus, has been found to cause impaired ability to maintain intact mucosal membrane functions and prevent leakage of toxins — bacterial endotoxins, as well as whole bacteria or debris of bacteria, the DNA of which are commonly found in most cells of the body, often in adipocytes of obese individuals or in arteriosclerotic plaques. Foods rich in proteotoxins such as gluten, casein and zein, and proteins, have been observed to have endotoxin-like effects that can contribute to dysbiosis. About 75% of the food in the Western diet is of limited or no benefit to the microbiota in the lower gut. Most of it, comprised specifically of refined carbohydrates, is already absorbed in the upper part of the GI tract, and what eventually reaches the large intestine is of limited value, as it contains only small amounts of the minerals, vitamins and other nutrients necessary for maintenance of the microbiota. The consequence is that the microbiota of modern humans is greatly reduced, both in terms of numbers and diversity when compared to the diets of our paleolithic forebears and the individuals living a rural lifestyle today. It is the artificial treatment provided in modern medical care — unfortunately often the only alternative provided — which constitute the main contributors to a poor outcome. These treatments include artificial ventilation, artificial nutrition, hygienic measures, use of skin-penetrating devices, tubes and catheters, frequent use of pharmaceuticals; they are all known to severely impair the microbiomes in various locations of the body, which, to a large extent, are ultimately responsible for a poor outcome. Attempts to reconstitute a normal microbiome by supply of probiotics have often failed as they are almost always undertaken as a complement to — and not as an alternative to — existing treatment schemes, especially those based on antibiotics, but also other pharmaceuticals.

About 25 million individuals undergo high risk surgery each year. Of these about 3 million will never return home from hospital, and the quality of life for many of those who return is often significantly impaired. Furthermore, many of those who manage to leave hospital have undergone severe life-threatening complications, mostly infections/sepsis. The development is strongly associated with the level of systemic inflammation in the body, which again is entirely a result of malfunctioning GI microbiota, a condition called dysbiosis, with deranged composition and function of the gastrointestinal microbiota from the mouth to the anus and impaired ability to maintain intact mucosal membrane functions and prevent leakage of toxins-bacterial endotoxins and whole or debris of bacteria, but also foods containing proteotoxins gluten, casein and zein and heat-induced molecules such as advanced glycation end products (AGEs) and advanced lipoxidation end products (ALEs). Markedly lower total anaerobic bacterial counts, particularly of the beneficial Bifidobacterium and Lactobacillus and higher counts of total facultative anaerobes such as Staphylococcus and Pseudomonas are often observed when analyzing the colonic microbiota. In addition Gram-negative facultative anaerobes are commonly identified microbial organisms in mesenteric lymph nodes and at serosal “scrapings” at laparotomy in patients suffering what is called “Systemic inflammation response system” (SIRS). Clearly the outcome is influenced by preexisting conditions in those undergoing surgery, but not to the extent as one could expect. Several studies have for example been unable to find significant influence of pre-existing obesity. The outcome seems much more to be related to the life-style of the individual and her/his “maintenance” of the microbiota e.g., size and diversity of microbiota, normal microbiota, eubiosis, being highly preventive.

Liver regeneration is a prerequisite for extended liver surgery. Several studies have shown that the bacterial gut flora is able to modulate liver function. Previously we observed that synbiotics could partly reverse the impaired mitosis rate of hepatocytes in a rat model of synchronous liver resection and colon anastomosis. The effect of synbiotics on liver function after hepatic resection has not been analysed yet. A prospective randomised double-blind pilot trial was undertaken in 19 patients scheduled for right hepatectomy. All patients received enteral nutrition immediately post-operatively. Comparison was made between a group receiving a combination of four probiotics and four fibres and a placebo group receiving the fibres only starting the day before surgery and continuing for 10 days. Primary study endpoint was the liver function capacity measured by ¹³C-methacetin breath test and indocyanine green plasma disappearance rate. Portal vein flow, liver volumetry, laboratory parameters for liver function, length of hospital stay, post-operative complications and side effects of synbiotic therapy were recorded. Liver function capacity was comparable in both groups. Complications had a negative impact on liver function. Because complications were more severe in the verum group, a sub-analysis was performed. In case of an uncomplicated course, liver function capacity was better in the patients with synbiotics. No severe side effects occurred. Synbiotics might be able to increase liver function capacity in patients after liver resection, but patient numbers were too small and the clinical courses too heterogeneous to draw any definite conclusions.

Background: Infection with HIV-1 results in marked immunologic insults and structural damage to the intestinal mucosa, including compromised barrier function. While the development of highly active antiretroviral therapy (HAART) has been a major advancement in the treatment of HIV-1 infection, the need for novel complementary interventions to help restore intestinal structural and functional integrity remains unmet. Known properties of pre-, pro-, and synbiotics suggest that they may be useful tools in achieving this goal. Methods: This was a 4-week parallel, placebo-controlled, randomized pilot trial in HIV-infected women on antiretroviral therapy. A synbiotic formulation (Synbiotic 2000®) containing 4 strains of probiotic bacteria (10¹⁰ each) plus 4 nondigestible, fermentable dietary fibers (2.5 g each) was provided each day, versus a fiber-only placebo formulation. The primary outcome was bacterial translocation. Secondary outcomes included the levels of supplemented bacteria in stool, the activation phenotype of peripheral T-cells and monocytes, and plasma levels of C-reactive protein and soluble CD14. Results: Microbial translocation, as measured by plasma bacterial 16S ribosomal DNA concentration, was not altered by synbiotic treatment. In contrast, the synbiotic formulation resulted in significantly elevated levels of supplemented probiotic bacterial strains in stool, including L. plantarum and P. pentosaceus, with the colonization of these two species being positively correlated with each other. T-cell activation phenotype of peripheral blood lymphocytes showed modest changes in response to synbiotic exposure, with HLA-DR expression slightly elevated on a minor population of CD4+ T-cells which lack expression of HLA-DR or PD-1. In addition, CD38 expression on CD8+ T-cells was slightly lower in the fiber-only group. Plasma levels of soluble CD14 and C-reactive protein were unaffected by synbiotic treatment in this study. Conclusions: Synbiotic treatment for 4 weeks can successfully augment the levels of probiotic species in the gut during chronic HIV-1 infection. Associated changes in microbial translocation appear to be absent, and markers of systemic immune activation appear largely unchanged. These findings may help inform future studies aimed at testing pre- and probiotic approaches to improve gut function and mucosal immunity in chronic HIV-1 infection. Trial registration: Clinical Trials.gov: NCT00688311