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Ginger is anti-cancer while Fluorine is carcinogenic

Dr. Olree says that Fluorine causes more cancer than any other mineral. Iodine prevents more cancer than any other mineral. Now we are finding that fluoridation of water is causing hypothyroidism to rise by thirty percent of more.

We have less iodine in our soils and thus less in our food as time goes on. Add to that the Cesium still being released into the Pacific Ocean from Fukashima every day since about this time four years ago and we have a “lack of Iodine crisis” in this country.

By the way, the price of Iodine almost doubled after the “event” in Japan. The “common knowledge” is that Iodine will remove radiation from the body. True, but a very expensive way to go about it. Boron is the only mineral that can accept radiation of all forms and not change it’s electron/neutron balance. It just attaches to the radiation and escorts it out of the body. Boron is how the Russians put out the “fire” of Chernoble.

Back to the Iodine. It is in the Halide group (Fluorine, Bromine, Chlorine and Fluorine in order from heavies mineral to lightest mineral). If the body has enough Iodine to use for all of the bodily functions (and we have been using Iodine in overdrive since Fukashima, depleting our bodies), it will simply excrete the other three that cause soooo much trouble in the body (we do need minimal amounts, but if you attempted to never eat any of those three, you would stay sufficient simply as a function of nature). If we lack Iodine the body tries to use the other three, the body  either says “wrong” and throws that attempt away and tries again (premature aging) or, if the body’s tumor suppressing genes malfunction, disease sets in.

Buy clean, local, regenerative food… and Ginger!

A new study reveals ginger contains a pungent compound that could be up to 10,000 times more effective than conventional chemotherapy in targeting the cancer stem cells at the root of cancer malignancy. 

A new study published in PLoS reveals a pungent component within ginger known as 6-shogaol is superior to conventional chemotherapy in targeting the root cause of breast cancer malignancy: namely, the breast cancer stem cells.

Vitamin K2 affects heart, bones and teeth and Vitamin A and D absorption

Vitamin K2 activates the proteins that vitamins A and D “tell” the cells to make, thus greatly increasing their effectiveness. This has huge implications for calcium metabolism, removing it from the body where it is the “hard” in hardening of the arteries as well as the culprit in spurs, and moving it to the bones and teeth, thus preventing dental decay and osteoporosis (these three are biochemically linked: cardiovascular health, bone health and dental health). Dietary intake of vitamin directly correlates with heart disease.

Vitamin K sources: grass-fed butter,

  • Green leafy vegetables, such as kale, spinach, turnip greens, collards, Swiss chard, mustard greens, parsley, romaine, and green leaf lettuce.
  • Vegetables such as Brussels sprouts, broccoli, cauliflower, and cabbage.
  • Fish, liver, meat, eggs, and cereals (contain smaller amounts)

Butyrate from fermented carbs

Anti-inflammation

Intestinal epithelium maintains a low grade of inflammation in order to prepare for constant immunological challenges on the mucosal surface (48, 61). If the immunological control is disrupted, the enterocytes might suffer from inflammatory and oxidative damages and even cause cancer (62, 63). Many studies have shown that butyrate can act as an anti-inflammatory agent. Several human and animal studies reported that the proinflammatory cytokines IFN-γ, TNF-α, IL-1β, IL-6, and IL-8 are inhibited, whereas IL-10 and TGF-β are upregulated in response to butyrate (25). The mechanism underlying the anti-inflammatory effect of butyrate is at least in part due to inhibition of the activation of a transcription factor known as NF-κB (64). NF-κB is a transcription factor that regulates the expression of a variety of genes involved in inflammation and immunity, such as proinflammatory cytokines and enzymes, adhesion molecules, growth factors, acute-phase proteins, and immune receptors (48, 65). Several studies suggested that butyrate suppresses the NF-κB signaling pathways by rescuing the redox machinery and controlling reactive oxygen species, which mediates NF-κB activation (66). Further studies also showed that butyrate is capable of activating PPAR-γ (67), which is a member of the nuclear hormone receptor family and highly expressed in colonic epithelial cells, and its activation is thought to exert anti-inflammatory effects (68). Apart from the inhibition of NF-κB activation and upregulation of PPAR-γ, butyrate may also exert its anti-inflammatory activities through inhibition of IFN-γ signaling (69).

Butyrate and the intestinal barrier

The barrier function of intestinal epithelial cells is an important first line of defense and ensures appropriate permeability characteristics of the epithelial layer (3, 70). Butyrate is known to repair and enhance barrier function of intestinal epithelial cells (71, 72). A current study by Elamin et al. (73) showed that butyrate exerts a protective effect on intestinal barrier function in Caco-2 cell monolayers. For example, butyrate is capable of upregulating the expression of mucin 2 (MUC2) (74), which is the most prominent mucin on the intestinal mucosal surface and can reinforce the mucous layer, leading to the enhanced protection against luminal pathogens (1, 74). In addition, the expression of trefoil factors (TFFs), which are mucin-associated peptides that contribute to the maintenance and repair of the intestinal mucosa (12), can be increased by butyrate (75). Furthermore, butyrate modulates the expression of tight junction proteins to minimize paracellular permeability (62, 76). One of several mechanisms in which butyrate enhances barrier function is through activation of AMP-activated protein kinase in monolayers (77). Butyrate can also stimulate the production of antimicrobial peptides, such as LL-37 in humans (78). However, on the basis of in vitro models, Huang et al. (79) showed that the effect of butyrate on the intestinal barrier function may be concentration-dependent. Butyrate promotes intestinal barrier function at low concentrations (≤2 mM) (77) but may disrupt intestinal barrier function by inducing apoptosis at high concentrations (5 or 8 mM) (79). On the basis of the physiologic concentration in mammalian gastrointestinal tract, the recommended concentration of butyrate used in in vitro models is currently 0–8 mM (80). However, considering that the majority of butyrate is metabolized as energy substrate by the colonic epithelium (12), the dosages used for treatment may be quite different between in vivo and in vitro models (4). For example, a dose of 100 mM butyrate by rectal administration was commonly used in clinical practice, which is comparable with physiologic concentrations in the colon of humans after the consumption of a high-fiber diet (81).

Butyrate and intestinal mucosal immunity

In addition to anti-inflammatory properties, SCFAs, especially butyrate, can act as modulators of chemotaxis and adhesion of immune cells (61). Butyrate can modulate intestinal epithelial cell–mediated migration of neutrophils to inflammatory sites, and such an effect is concentration-dependent (82, 83). In addition, butyrate plays a role in cell proliferation and apoptosis. Butyrate stimulates cell growth and DNA synthesis and induces growth arrest in the G1 phase of the cell cycle (5, 61). Although low concentrations of butyrate enhance cell proliferation (5), high concentrations of butyrate induce apoptosis (57). Overall, butyrate can influence the immune response by affecting immune cell migration, adhesion, and cellular functions such as proliferation and apoptosis.

Butyrate and Obesity: Inhibition or Promotion?

The abnormalities in glycolipid metabolism are a main reason for obesity, diabetes, and other metabolic syndromes (84). So far, the effect of butyrate on glycolipid metabolism remains controversial. We summarized the experimental studies that evaluated the potential relation between butyrate and obesity.

A growing body of evidence indicates extensive communications between the brain and the gut via the gut-brain axis (115, 116). The gut-brain axis is composed of the central nervous system, enteric nervous system, and different types of afferent and efferent neurons that are involved in signal transduction between the brain and gut (15, 117). The bidirectional communication between the gut and the brain occurs through various pathways, including the vagus nerve, neuroimmune pathways, and neuroendocrine pathways (118, 119). As a microbial metabolite, butyrate is capable of exerting its effects on host metabolism indirectly by acting through the gut-brain axis (114, 120). For instance, butyrate can enhance the proportion of cholinergic enteric neurons via epigenetic mechanisms (121). Moreover, with an ability to cross the blood-brain barrier, butyrate activates the vagus nerve and hypothalamus, thus indirectly affecting host appetite and eating behavior (122, 123). Some of the beneficial metabolic effects of butyrate are mediated through gluconeogenesis from the gut epithelium and through a gut-brain neural circuit to increase insulin sensitivity and glucose tolerance (124, 125). For example, butyrate binds to its receptor in the intestinal cells and signals to the brain through the cAMP signaling pathway (126, 127).

Fruits and Vegetables

Consumption of fruits and vegetables such as green beans, legumes, leafy greens, apples, kiwi and oranges might also increase the plasma butyrate content because of increased fiber content. Fruits also provide several vitamins and minerals and are one of the best and healthy sources of butyrate.

Impacts of Macronutrients on the Gut Microbiota – carbohydrate

Substrate Supply to the Colonic Microbiota

An adult colon contains approximately 500 g of contents, most of which is bacteria [], and about 100 g/day is voided as stool. A typical western type diet supplies the colonic microbiota with about 50 g daily of potentially fermentable substrate, predominantly dietary fiber (DF). Non-starch polysaccharides (NSP) are major components of DF and account for 20%–45% of the dry matter supplied to the colon. Simple sugars and oligosaccharides each represent a further 10% whereas starch (and starch hydrolysis products) supplies less than 8% of dry matter. Some sugar alcohols also escape small intestine (SI) absorption and are minor dietary substrates for the colonic microbiota []. About 5–15 g of protein and 5–10 g of lipid passes into the proximal colon daily, largely of dietary origin. Various other minor dietary constituents, including polyphenols, catechins, lignin, tannins and micronutrients also nourish colonic microbes. About 90% of the approximately 1 g/day of dietary polyphenols escapes digestion and absorption in the SI [,] and can have significant influence on microbial populations and activities [,,].

Carbohydrates—Importance for Large Bowel Fermentation and Health

Carbohydrates are the principal carbon and energy source for colonic microbes. Collectively, they have an immense capacity to hydrolyse a vast range of these nutrients, especially complex polysaccharides [].

DF is integral to a healthy diet and Australian adults consume ~27 g each day [], which is greater than in other high income countries, including the USA (<20 g/day). Epidemiological and experimental studies show that DF is both preventative and therapeutic for many large bowel disorders and other conditions or diseases, including cardiovascular diseases, type II diabetes and obesity [,,,,].

One mechanism by which fiber promotes and maintains bowel health is through increasing digesta mass. Incompletely fermented fiber (e.g., insoluble NSP such as cellulose), increases digesta mass primarily though its physical presence and ability to adsorb water. An increase in digesta mass dilutes toxins, reduces intracolonic pressure, shortens transit time and increases defecation frequency. Fibers can also increase fecal mass to a lesser degree by stimulating fermentation, which leads to bacterial proliferation and increased biomass [].

Many of the health benefits ascribed to fiber are a consequence of their fermentation by the colonic microbiota and the metabolites that are produced. Carbohydrates are fermented to organic acids that provide energy for other bacteria, the bowel epithelium and peripheral tissues. SCFA are the major endproducts of carbohydrate fermentation. These weak acids (pKa ~4.8) help lower the pH within the colon thereby inhibiting the growth and activity of pathogenic bacteria. Other minor organic acids produced include lactate, succinate and formate. Branched-chain SCFA (e.g., isobutyrate and isovalerate) results from fermentation of branched chain amino acids [].

There are spatial gradients in microorganisms along the length of the gut. Bacterial growth and metabolic activity (fermentation) is greatest in the proximal colon where substrate availability is at a maximum [,]. Accordingly, pH progressively increases as stool progresses from the proximal to distal colon (from 5.8 to 7.0–7.5), largely because of the progressive depletion of carbohydrate substrates and absorption of SCFA, and increasing efficiency of protein fermentation and production of alkaline metabolites []. Total SCFA concentrations are highest in the proximal colon (~100 mM) and decline progressively toward the distal colon. Acetate, propionate and butyrate are the major individual SCFA, accounting for 90% of the total, with molar ratios approximating 65:20:15 [].

Butyrate has attracted significant attention because it serves as the principal source of metabolic energy for the colonocytes [], is instrumental in maintaining mucosal integrity, modulates intestinal inflammation and promotes genomic stability. The capacity of butyrate to regulate colonocyte differentiation and apoptosis, promoting removal of dysfunctional cells, underscores its potential to protect against colon cancer [].

The SCFA also have roles beyond the gut and may improve risk of metabolic and immune system diseases and disorders, such as osteoarthritis, obesity, type II diabetes and cardiovascular disease [,].

More than 90% of the total SCFA produced in the colon is absorbed by the epithelium, through mechanisms that are not fully elucidated. SCFA-stimulated sodium-coupled transport in the apical membrane of colonocytes is especially important as it mediates (co)absorption of water and helps recover electrolytes as well as energy []. The SCFA can bind to G-protein coupled receptors in colorectal tissues, particularly GPR 41 and 43, which may influence immune function and tumour suppression, but these pathways are still relatively poorly characterized [].

Most of the absorbed acetate reaches the liver via the portal vein, whereas propionate, and butyrate to an even larger extent, is metabolized extensively by colonocytes. Acetate and propionate are used by the liver for oxidation, and for lipogenesis and gluconeogenesis, respectively. Hepatic metabolic clearance of SCFA is very high and so concentrations in the systemic bloodstream are about 100-fold lower than those in colonic digesta and feces (~50 µM versus 100 mM, respectively) [].

Gut Bacteria Influences Metabolism – fermented carbohydates

Gut Bacteria Influences Metabolism Through the Immune System

Summary: Digestive enteroendocrine cells use an innate immune pathway to respond to good bacteria by fine tuning metabolism to diet and intestinal conditions, a new study reveals.

Source: Boston Children’s Hospital.

Research tells us that the commensal or “good” bacteria that inhabit our intestines help to regulate our metabolism. A new study in fruit flies, published June 21 in Cell Metabolism, shows one surprising way they do this.

The study, led by Paula Watnick, MD, PhD, of the Division of Infectious Diseases at Boston Children’s Hospital, reveals that innate immune pathways, best known as our first line of defense against bacterial infection, have a side job that’s equally important.

In the intestine, digestive cells use an innate immune pathway to respond to harmful bacteria. But other intestinal cells, enteroendocrine cells, use the same pathway, known as IMD, to respond to “good” bacteria — by fine-tuning body metabolism to diet and intestinal conditions.

“Some innate immune pathways aren’t just for innate immunity,” says Watnick. “Innate immune pathways are also listening to the ‘good’ bacteria — and responding metabolically.”

Metabolic syndrome, fatty liver in flies

Watnick and her colleagues knew from their previous research that bacteria living in flies’ intestines make a short-chain fatty acid, acetate, that is essential for the flies’ own lipid metabolism and insulin signaling. Flies with no bacteria in their intestines (and hence, no acetate) accumulated fat droplets in their digestive cells. The lab of Norbert Perrimon, PhD, at Harvard Medical School had previously found similar fat droplets in flies whose enteroendocrine cells lacked tachykinin, an insulin-like protein important in growth, lipid metabolism and insulin signaling.

“When there’s a problem processing glucose or lipids, fats get stuck in these droplets in cells that are not designed for fat storage,” she says.

The new study again used fruit flies, which are easy to breed and manipulate genetically, and have cell types in their intestines much like humans’. When Watnick and colleagues examined flies with mutations in the IMD innate immune pathway, they again saw fat droplets in their intestines.

Watnick believes these fat droplets, whether caused by loss of intestinal bacteria, loss of tachykinin or loss of the innate immune pathway, are the equivalent of fatty liver. Their accumulation is a sign that the body cannot properly metabolize carbohydrates and fats. In essence, Watnick thinks these flies have metabolic syndrome, commonly associated with obesity and type 1 diabetes.

Defining the immune system’s role in metabolism

How are intestinal bacteria, the innate immune system and metabolism related? Through a series of experiments, the team began to tease out exactly how bacteria exert their metabolic influence. They showed that:

  • The innate immune pathway spurs enteroendocrine cells to produce tachykinin.
  • In the absence of either bacteria or their breakdown product, acetate, no tachykinin is made.
  • When germ-free flies are given acetate, the innate immune pathway is reactivated and their metabolism normalizes.
  • A specific innate immune receptor on enteroendocrine cells, PGRP-LC, is required to receive the acetate signal.

“We know bacteria control our metabolism, but no one realized that bacteria were interacting with innate immune signaling pathways in enteroendocrine cells,” says Watnick. “Maybe these pathways are really a system that allows cells to recognize bacteria for different reasons.”

A two-pronged interaction

The study also showed that activation of the innate immune pathway in enteroendocrine cells is essential for normal fly growth and development. When Watnick and colleagues inactivated the pathway, they got growth-stunted flies. Feeding the flies acetate or directly reactivating the innate immune pathway got them growing again.

a fly and bacteria

Though Watnick would now like to confirm these findings in a mammalian model, the study further sketches out what appears to be a two-pronged interaction between our microbiome and our metabolism. Good bacteria ferment nutrients in our diet and release short-chain fatty acids like acetate, which help us optimize our use and storage of nutrients. Pathogenic “bad” bacteria do the opposite: They consume fatty acids, impeding healthful metabolism. An imbalance in our intestinal microbiome has been linked to obesity and sometimes contributes to malnutrition. (More in this comprehensive review article authored by Watnick with lab members Adam Wong and Audrey Vanhove).

And because acetate is produced through fermentation, Watnick and colleagues speculate that eating more fermentable carbohydrates may boost acetate levels and promote good metabolism. Such foods may help counteract imbalances in our gut bacteria, such as those caused by protracted antibiotic use, they suggest.

Fermented Beet Cauliflower

Ingredients

  • 1 head cauliflower
  • 2 large beets, peeled and cut into chunks
  • Salt (2 Tablespoons per litre of water)
  • Peeled garlic
  • Cumin seeds
  • Chilli flakes
  • Water
  1. Mix 2 tablespoons of salt per litre of water, and stir until all the salt is dissolved.
  2. Break the cauliflower into chunks and cut or leave the garlic whole. Tightly pack the vegetables into a glass jar, and add cumin seeds and chilli flakes.
  3. Pour the salty water/brine over the vegetables. All the vegetables should be fully submerged into the brine. To keep everything under, place a small glass filled with the brine on top. Cover the jar with a lid or cloth and let it ferment for 4-6 weeks.
  4. Adding some sauerkraut or other fermented veggie juice helps speed up the fermentation process but it’s not necessary so don’t worry if you haven’t got any.

Cook your fish to kill parasites

Consumption of fluke-free fish is the most important factor in controlling Opisthorchis viverrini (OV) infection in endemic areas such as northeast Thailand and thereby reducing the risk of cholangiocarcinoma. Cooking fish is the best way to avoid infection; however, the cultural practice of eating raw or fermented fish is difficult to change. We investigated the food preparation process, using freezing, heating and fermentation to kill OV metacercariae in fish.

Uncooked cyprinid fish infected with OV were divided into three groups: refrigerated at 4 oC for 24, 48 or 72 h (control group); frozen at -20 oC for 24, 48 or 72 h; or heated by microwaving (at 400 or 800 W) or boiling at 90 oC for 1, 5 or 10 min. Moreover, pickled (fermented) fish were divided into two groups: refrigerated at 4 oC (control) or frozen at -20 oC for 24 or 48 h. The infectivity of recovered metacercariae was confirmed by infecting hamsters with OV and then evaluating the recovery of adult worms after 1 month. We found that a heating process, by boiling or microwaving at 400 or 800 W for at least 5 min, could kill OV metacercariae, and freezing pickled fish at -20 oC for 48 h could kill OV metacercariae in all sizes of fish. The present study found that heating and freezing processes, as well as the fermentation process under optimal conditions, could kill OV metacercariae in a timely manner. This knowledge is valuable for implementation in endemic areas to control OV infection and cholangiocarcinoma.

In conclusion, heating at 70 and 80°C groups after 10, 15, and 30 min can kill O. viverrini eggs. This study suggests that destroying the Opisthorchis viverrini eggs in feces using heat is a possible approach for controlling egg contamination in the environment.

 

Microwaving at 400 or 800 W for at least 5 min, could kill OV metacercariae.

PATHOGENICITY/TOXICITY: There is consensus that the biology and pathologic characteristics of Opisthorchis and Clonorchis are the same, essentially low grade biliary tract pathogens.  The majority of Opisthorchis infections (around 80%) are light infections Footnote1Footnote2. Classified by less than 1000 eggs/g of feces, a light infection is usually asymptomatic except for eosinophilia Footnote2. With this stage, there is no noticeable damage to liver function Footnote2. A heavy infection is classified by 10,000-30,000 eggs/g of feces Footnote2. The clinical presentation of a heavy infection includes diarrhea, constipation, abdominal pain, anorexia, indigestion, gastrointestinal bleeding, lassitude, mild fever, jaundice, enlarged or non-functional gall bladder, cholecystitis, cholangitis, liver abscess, and gallstones Footnote2Footnote3Footnote7. Clinical presentation of untreated chronic infection includes oedema of the legs, ascites, mild cirrhosis, hepatomegaly, and biliary epithelium hyperplasia and inflammation Footnote2. Cholangiocarcinoma is strongly associated with O. viverrini infection and has a high mortality rate Footnote2. It usually develops 30-40 years after initial infection, and its victims usually die within 3-6 months Footnote2Footnote8.

EPIDEMIOLOGY: O. viverrini is endemic in Thailand, Laos, and Cambodia. O. felineus is reported in North Europe and Asia Footnote2. Infection is more common from September to February. In endemic areas, infection rates can be up to 90% in humans, and 97% in fish Footnote5. Infection is uncommon in children under 5 years of age. Prevalence of Opisthorchiasis is higher in areas that are poor or unsanitary Footnote9Footnote10.

HOST RANGE: Humans, snails, fish, cats, dogs, reptiles, amphibians, and fish-eating animals Footnote4Footnote11-13

INFECTIOUS DOSE: Possibly as low as 1-2 metacercariae Footnote8.

MODE OF TRANSMISSION: Opisthorchis spp. are transmitted when raw or undercooked fish containing metacercariae is ingested Footnote3.

Parasites that can lead to cancer

 

Certain parasitic worms that can live inside the human body can also raise the risk of developing some kinds of cancer. These organisms are not found in the United States, but they can be a concern for people who live in or travel to other parts of the world.

Opisthorchis viverrini and Clonorchis sinensis are liver flukes (a type of flatworm) that have been linked to increased risk of developing cancer of the bile ducts. The bile ducts are tubes that connect the liver to the intestines. These infections come from eating raw or undercooked freshwater fish. They occur mostly in East Asia and are rare in other parts of the world.

Schistosoma haematobium is a parasite found in the water of some countries in the Middle East, Africa, and Asia. Infection with this parasite (an illness called schistosomiasis) has been linked to bladder cancer. Possible links to other types of cancer are now being studied as well.

Tips when taking probiotics

  1. Always choose a probiotic supplement with at least 10 billion live organisms per dosage. Keep in mind that the probiotic supplement should ensure (in writing) that you’ll continue to receive this number throughout the shelf life of the product.
  2. Avoid taking probiotics with chlorinated water. Chlorine is added to municipal water systems to kill bacteria, and this could very well impact the effectiveness of your probiotic supplement.
  3. Probiotics are best consumed on an empty stomach, when stomach acid levels are lower.
  4. Make sure you provide a nurturing environment for your probiotic organisms by consuming adequate amounts of prebiotic fiber. Foods rich in prebiotic fiber include jicama, dandelion greens, onions, garlic leeks, and there are terrific prebiotic supplements available as well. Look for supplements made from acacia gum and baobab fruit as they are highly effective and well tolerated.
  5. Look for probiotics with a wide array of different bacteria. There are now some excellent products that contain 14 different strains. Keep in mind that there are five key organisms that should certainly be a part of any probiotic that you may choose. These include:
  • Lactobaccilus plantarum: Found in kimchi, sauerkraut, and other cultured vegetables, this bug is one of the most beneficial bacteria in your body. It survives in the stomach for a long time and performs many functions that help regulate immunity and control inflammation in the gut. It also helps fortify the gut lining, fending off potential invaders that might compromise the intestinal wall and sneak into the bloodstream. In fact, plantarum’s beneficial impact on the gut lining is perhaps its most important attribute, for it reduces gut permeability, thereby reducing the associated risks for leaky gut—including an increased risk for virtually every brain disorder. Moreover, L. plantarum can quickly digest protein, and this may reduce food allergies and even treat such allergies when they arise. It’s been shown in experimental animal studies to protect engineered mice from having clinical symptoms of multiple sclerosis and even reduce the inflammatory response typical of that condition. Finally, L. plantarum has an uncanny ability to absorb and maintain important nutrients such as brain-friendly omega-3 fatty acids, vitamins and antioxidants. All of these actions make L. plantarumessential for fighting infection and taking control of any pathogenic bacteria.
  • Lactobaccilus acidophilus: acidophilus is the darling of fermented dairy products, including yogurt. It keeps the balance of good vs. bad bacteria in check and in doing so, aids your immune system. In women, it helps to curb the growth of Candida albicans, a fungus that can cause yeast infections. L. acidophilus has also gained fame for its ability to help maintain cholesterol levels. In the small intestine, L. acidophilusproduces many beneficial substances that combat pathogenic microbes, including acidolphilin, acidolin, bacteriocin, and lactocidin.
  • Lactobaccilus brevis: Sauerkraut and pickles owe a lot of their benefits to this bug, which improves immune function by increasing cellular immunity and even enhancing killer T cell activity. It’s so effective in combating vaginosis, a common bacterial infection of the vagina, that it’s added to pharmaceuticals used to treat it. brevis also acts to inhibit the effects of certain gut pathogens. Perhaps best of all, it has been shown to increase levels of that all-star brain growth hormone BDNF.
  • Bifidobacterium lactis (also called animalis): Fermented milk products like yogurt contain this gem, which is well documented to have a powerful effect on preventing digestive ills and boosting immunity. It’s also known to be helpful in knocking out foodborne pathogens like salmonella, which causes diarrhea.
  • Bifidobacterium longum: Just one of the 32 species that belong to the genus bifidobacterium, this is one of the first bugs that colonize our bodies at birth. It has been associated with improving lactose tolerance and preventing diarrhea, food allergies and the proliferation of pathogens. It’s also known to have antioxidant properties as well as the ability to scavenge free radicals. In laboratory mice, longumhas been shown to reduce anxiety. Like L. acidophilus, B. longum also helps maintain healthy cholesterol levels.

Circadian clock alters response to diet and changes to gut microbiome

Image shows a head with the brain exposed.

PARKINSON’S ASSOCIATED PROTEIN LINKED TO HUMAN UPPER GI TRACT INFECTIONS

NEUROSCIENCE NEWS
A new study reports chronic infections of the upper gastrointestinal tract could be linked to Parkinson’s disease. Researchers say alpha synuclein, a Parkinson’s linked protein, is released during upper GI infections, inducing an immune response. Findings suggest frequent chronic infections could overwhelm the body’s ability to remove the protein, leading to the onset of Parkinson’s.… READ MORE…
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Traumatic brain injury causes intestinal damage

Image shows a head with the brain exposed.

PARKINSON’S ASSOCIATED PROTEIN LINKED TO HUMAN UPPER GI TRACT INFECTIONS

NEUROSCIENCE NEWS
A new study reports chronic infections of the upper gastrointestinal tract could be linked to Parkinson’s disease. Researchers say alpha synuclein, a Parkinson’s linked protein, is released during upper GI infections, inducing an immune response. Findings suggest frequent chronic infections could overwhelm the body’s ability to remove the protein, leading to the onset of Parkinson’s.… READ MORE…
FEATUREDNEUROLOGYOPEN NEUROSCIENCE ARTICLES8 MIN READ

Bacteria in fermented food signal the immune system

This shows a diagram of the gut

BACTERIA IN FERMENTED FOOD SIGNAL THE HUMAN IMMUNE SYSTEM, EXPLAINING HEALTH BENEFITS

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A metabolite produced by lactic acid bacteria binds to the third hydroxycarboxylic acid receptor (HCA), signalling the immune system. Researchers believe the receptor evolved to allow great apes to consume foods that were starting to decay. They suggest the receptor could mediate some beneficial and anti-inflammatory effects of lactic acid in humans, and could serve as a target to treat inflammatory diseases.… READ MORE…
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This shows a sad looking child in a garden

GASTROINTESTINAL COMPLAINTS IN CHILDREN COULD SIGNAL FUTURE MENTAL HEALTH PROBLEM

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A correlation between gastrointestinal symptoms, adversity and childhood anxiety has been identified by researchers at Columbia University. Studying fMRI data and fecal samples, researchers noted adversity was associated with microbial diversity changes and differences prefrontal cortex activation in response to emotional faces.… READ MORE…
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Study links gut bacteria that can lead to seizures and strokes

Delaying age related diseases by keeping gut bacteria in balance

intestines

MICROBIAL BASED TREATMENT REVERSES ASD’S SOCIAL DEFICITS: MOUSE STUDY

NEUROSCIENCE NEWS
Researchers report the administration of Lactobacillus reuteri may lead to brain changes that reverse social deficits in mouse models of ASD through a mechanism that involves the vagus nerve and reward system. The findings hold promise for the development of treatments for ASD, as well as other disorders, by modulating specific gut microbes.… READ MORE…
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This shows a brain and a stomach

AUTISM SYMPTOMS REDUCED NEARLY 50% TWO YEARS AFTER FECAL TRANSPLANT

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Arizona State University researchers claim microbiota transfer therapy reduces symptoms associated with autism and gastrointestinal problems for two years post-treatment. The study suggests MTT may be a promising option for helping to treat children with ASD who also have GI problems. The researchers stress further research, including double-blind, placebo-controlled randomized trials with a larger cohort be carried out. … READ MORE…
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More sociable chimps harbor richer gut microbiomes

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