Lemon grass or Tanglad to fight insomia

The health benefits of lemongrass include relief from stomach disorders, insomnia, respiratory disorders, fever, aches, infections, rheumatism and edema. The defensive antioxidant activity of the lemongrass herb protects against antibiotic-resistant Staphylococcus aureus and helps in maintaining optimum cholesterol levels, cellular health, nervous system, healthy skin and immune system. It is also effective in treating type 2 diabetes, cancer, and obesity, while also aiding in detoxification. It is extensively used in aromatherapy and helps to combat fatigue, anxiety and body odor.

Lemongrass – An Aromatic Healer

Cymbopogon citratus also known as Lemongrass is an herb which belongs to the grass family of Poaceae. It is well known and utilized for its distinct lemon flavor and citrusy aroma. It is a tall, perennial grass which is native to India and tropical regions of Asia. It is a coarse and tufted plant with linear leaves that grows in thick bunches, emerging from a strong base and standing for about 3 meters in height with a meter-wide stretch.

In addition to its culinary usage, lemongrass offers a wide array of medicinal benefits and is in extensive demand due to its antibacterial, anti-fungal and antimicrobial properties across Southeast Asia, as well as the African and American continents.

The genus Cymbopogon comprises of 55 species of grass, two of which are referred to as Lemongrass. These are West Indian lemongrass or Cymbopogon citratus which is famously preferred for culinary use and East Indian lemongrass or Cymobopogon flexuosus which is used in the manufacturing of various products such as fragrances because of its extended shelf life, owing to the low amount of myrcene in that variety.

Nutritional Value Of Lemongrass

Lemongrass is an aromatic storehouse of essential nutrients providing a wide array of health benefits. It is a source of essential vitamins such as vitamin A, vitamin B1 (thiamine), vitamin B2 (riboflavin), vitamin B3 (niacin), vitamin B5 (pantothenic acid), vitamin B6 (pyridoxine), folate and vitamin C. It also provides essential minerals such as potassium, calcium, magnesium, phosphorous, manganese, copper, zinc and iron, which are required for the healthy functioning of the human body. It offers no harmful cholesterol or fats.

Health Benefits Of Lemongrass

Lemongrass contains antioxidants, flavonoids and phenolic compounds such as luteolin, glycosides, quercetin, kaempferol, elimicin, catecol, chlorogenic acid, and caffeic acid, all of which help in providing an impressive range of medicinal aids. The main componentof lemongrass is lemonal or citral, which has anti-fungal and antimicrobial qualities, while also providing a distinct lemony smell. Some of the most well known health benefits of lemongrass include:

Cholesterol: Lemongrass possesses anti-hyperlipidemic and anti-hypercholesterolemic properties that support healthy cholesterol levels. Studies have shown that the regular consumption of lemongrass has shown significant results in sustaining healthy levels of triglycerides and reducing the LDL cholesterol in the body. This helps in preventing the accumulation of lipids in the blood vessels and promotes the unobstructed flow of blood in the arteries and prevents various cardiac disorders such as atherosclerosis.

Detoxification: Lemongrass helps in cleansing and flushing harmful toxic wastes out of the body, as a result of its diuretic properties. Detoxification helps in better regulation of various organs of the body, including the liver and kidney, while also helping to lower the levels of uric acid. The diuretic effect of lemongrass helps in increasing the quantity and frequency of urination, which helps in maintaining digestive health, eliminating accrued fats, and assisting in maintaining a clean system.

lemongrassCancer: Lemongrass is effective in treating various types of cancers without affecting the healthy normal cells of the body. Research conducted to prove the anti-cancerous activity of lemongrass has shown promising outcomes in the prevention of skin cancer. Studies have shown that a certain component, citral, which is present in lemongrass, helps in inhibiting the growth of hepatic cancer cells during the initial phases and prevents any further production of cancerous cells. Another study has provided supporting evidence regarding the anti-proliferative effect of citral in impeding the growth of human breast cancer cells and the induction of apoptosis.

Staphylococcus aureus: Studies have shown that lemongrass essential oil has an anti-biofilm capacity and is beneficial against the infection caused by Staphylococcus aureus. It contains phenols which possess the capability to spread quickly through the body tissues and cure biofilms located anywhere in the body. It disrupts the growth and communication of germs which helps in inhibiting the formation of biofilms. The essential oil of lemongrass is useful for application both topically as well as internally in the diseases diagnosed with biofilms, such as Lyme disease.

Stomach Disorders: Studies have shown that lemongrass essential oil has anti-microbial and anti-bacterial properties which help in fighting the infections caused by various pathogens such as Helicobacter pylori and Escherichia coli. It is beneficial in the prevention of gastrointestinal disorders such as gastric ulcers, helps in stimulating the bowel function, and improves digestion. The anti-inflammatory properties of lemongrass are beneficial for treating constipation, ulcerative colitis, diarrhea, nausea and stomach aches.

Insomnia: Lemongrass aids in calming the muscles and nerves which helps in inducing deep sleep. Research has shown that lemongrass tea has sedative and hypnotic properties which help in increasing the duration and quality of sleep.

Respiratory Disorders: Lemongrass is widely used in Ayurvedic medicine for its healing effects in treating coughs and colds. Along with other beneficial components, the vitamin C content present in it helps in providing relief from nasal blockages, flu and other respiratory disorders such as bronchial asthma.

Fever: Lemongrass is a febrifuge and is also known as the ‘fever grass’, owing to its beneficial effects in lowering  fevers. The anti-pyretic and diaphoretic effect of lemongrass is extensively used in Ayurvedic medicine for curing fevers by inducing sweating.

Infections: Lemongrass works as an antiseptic and is effective in treating infections such as ringworm, sores, Athlete’s Foot, scabies, and urinary tract infections because of its antimicrobial and anti-fungal properties. Studies have shown that lemongrass exerts healing effects on dermatological infections, such as yeast infections, by inhibiting the growth of pathogens. Another study provided supporting evidence that demonstrated the efficacy of lemongrass over thyme, patchouli and cedar wood oil in the treatment of various diseases such as oral or vaginal candidias.

Aches: Lemongrass helps in alleviating the pain and discomfort caused by headaches and migraines due to its analgesic properties. The phytonutrients present in it improve the blood circulation and help in relieving spasms, muscle cramps, sprains, and back aches. It is valuable in treating sports wounds, including dislocations, internal injuries and bruises.

Nervous System: Lemongrass is a nervine and has been proven to be an  tonic for the nervous system. It stimulates the mind and helps in combating convulsions, nervousness, vertigo and various neuronal disorders such as Alzheimer’s and Parkinson’s disease. It is used in therapeutic baths, which assist in calming the nerves and help in alleviating the symptoms of anxiety and fatigue caused by stress.

Type-2 Diabetes: Lemongrass has been proven beneficial in treating Type-2 diabetes. Studies have shown that the citral present in it helps to maintain optimum levels of insulin and improves the tolerance of glucose in the body.

Rheumatism: Lemongrass is effective in relieving the pain and discomfort caused by rheumatism. It can be applied topically on both lumbago and sprains and helps in relieving neuralgia and other painful sufferings.

Immune System: Lemongrass helps in restoring the vital systems which are operational in the body, including digestion, respiration, excretion and nervous system. This assists in better absorption of nutrients and strengthens the immune defense mechanism of the body. Lemongrass extracts have a beneficial effect on the inflammatory actions of cytokines, which are the signaling molecules through which the cells communicate and respond in the body. Studies have shown that lemongrass exerts anti-inflammatory action and its constituents such as citral may be the cause behind its inhibitory effects on cytokine production.

Skin Care: Lemongrass has been treasured as a skin tonic and makes an effective cleanser for oily or acne-prone skin, due to its astringent and antiseptic qualities. It helps in strengthening the skin tissues and toning up the pores while also sterilizing them. Care should be taken while using lemongrass products, as the undiluted application might lead to dermal irritation in some cases.

Cellular Health: Lemongrass possesses antioxidant qualities and help in protecting the body cells from the oxygen-derived free radicals. It also helps in the cleansing of blood and strengthens the spleen to discard the tarnished red blood cells. It supports the function of the thymus glands which helps to produce white blood cells. It helps in stimulating regeneration of cells. The folate and potassium content in the stem and leaves of lemongrass aids in DNA synthesis and promotes cell division.

Edema: Lemongrass is effective in curing the condition of water retention or edema. It has a cleansing effect on lymphatic congestion and helps to soothe the swelling.

Social Experience Tweaks Genome Function to Modify Future Behavior

Summary: Researchers have identified the activity of a genetic network that responds to social stress in mice.

Source: University of Illinois.

Researchers at the University of Illinois are uncovering the genomic mechanisms that underlie social behavior in mice, some of which may be shared widely across animal species

Mice have a reputation for timidity. Yet when confronted with an unfamiliar peer, a mouse may respond by rearing, chasing, grappling, and biting–and come away with altered sensitivity toward future potential threats.

What changes in the brain of an animal when its behavior is altered by experience? Research at the University of Illinois led by Professor of Cell and Developmental Biology Lisa Stubbs is working toward an answer to this question by focusing on the collective actions of genes. In a recent Genome Research publication, Stubbs and her colleagues identified and documented the activity of networks of genes involved in the response to social stress.

“The goal of this study was to understand the downstream events in mice, and how they are conveyed across interacting brain regions . . . how they might set the stage for emotional learning in response to social threat,” said Stubbs. Answers to these questions could help scientists understand how the brains of other animals, including humans, generate social behavior, as well as what goes wrong in disorders of social behavior.

The new results are part of a large-scale research project funded by the Simons Foundation that is headed by Stubbs and includes many of her coauthors, including first authors Michael Saul and Christopher Seward. Stubbs, Saul, Seward, and other coauthors are members of the Carl R. Woese Institute for Genomic Biology (IGB); Saul is an IGB Fellow and Seward is a graduate student.

An aggressive encounter between two mice is just one strand of the web of interactions that connects a population of social animals. Like individuals in a community, the genes in a genome cannot be completely understood until their relationships to one another are examined in context, including how those relationships may change across different tissues and over time.

Stubbs’ team wanted to gather information that would allow them to construct this type of comprehensive gene network to reflect how the brain of a social animal responds to an aggressive encounter. They staged a controlled encounter between pairs of mice; one mouse in its home cage, and a second, unfamiliar mouse introduced behind a screen. The presence of the intruder mouse created a social challenge for the resident mouse, while the screen prevented a physical encounter.

The researchers then quantified the activity of genes in several different regions of the brain associated with social behaviors–the frontal cortex, hypothalamus, and amygdala–and at several time points in the two hours following the encounter. In analyses of the resulting data, they looked for groups of genes acting together. In particular, they sought to identify transcription factors, genes whose protein products help control other genes, that might be orchestrating the brain’s molecular response.

Stubbs was excited to discover that the results mirrored and expanded upon previous work in other species by collaborators at the IGB, including work by the laboratory of Director Gene Robinson in honey bees.

“As we examined the regulatory networks active in the mouse brain over time, we could see that some of the same pathways already explicated in honey bees… were also dysregulated similarly by social challenge in mice,” she said. “That cross-species concordance is extremely exciting, and opens new doors to experimentation that is not being pursued actively by other research groups.”

Among the genes responding to social challenge were many related to metabolism and neurochemical signaling. In general terms, it appeared that cells in the brains of challenged mice may alter the way they consume energy and communicate with one another, changes that could adjust the neural response to future social experiences.

The researchers looked for associations between genes’ responses to social experience and their epigenetic state. How different regions of DNA are packaged into the cell (sometimes referred to as chromatin structure) can influence the activity of genes, and so-called epigenetic modifications, changes to this structure, help to modify that activity in different situations.

Image shows a DNA strand.

“We found that the chromatin landscape is profoundly remodeled over a very short time in the brain regions responding to social challenge,” said Stubbs. “This is surprising because chromatin profiles are thought to be relatively stable in adult tissues over time.” Because such changes are stable, they are sometimes hypothesized to reinforce long-term behavioral responses to experience.

Stubbs and her colleagues hope that by identifying genomic mechanisms of social behavior that are basic enough to be shared even between distantly related animal species, they can discover which biological mechanisms are most central.

“The most exciting thing in my view is using [comparisons between species] to drill through the complex response in a particular species to the ‘core’ conserved functions,” she said, “thereby providing mechanistic hypotheses that we can follow by exploiting the power of genetic models like the mouse.”

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Funding: Funding provided by Simons Foundation.

Source: Nicholas Vasi – University of Illinois
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: Abstract for “Transcriptional regulatory dynamics drive coordinated metabolic and neural response to social challenge in mice” by Michael C. Saul, Christopher H. Seward, Joseph M. Troy, Huimin Zhang, Laura G. Sloofman, Xiaochen Lu, Patricia A. Weisner, Derek Caetano-Anolles, Hao Sun, Sihai Dave Zhao, Sriram Chandrasekaran, Saurabh Sinha, and Lisa Stubbs in Genome Research. Published online March 29 2017 doi:10.1101/gr.214221.116

CITE THIS NEUROSCIENCENEWS.COM ARTICLE
University of Illinois “Social Experience Tweaks Genome Function to Modify Future Behavior .” NeuroscienceNews. NeuroscienceNews, 7 June 2017.
<http://neurosciencenews.com/future-behavior-experience-genetics-6860/&gt;.

Abstract

Transcriptional regulatory dynamics drive coordinated metabolic and neural response to social challenge in mice

Agonistic encounters are powerful effectors of future behavior, and the ability to learn from this type of social challenge is an essential adaptive trait. We recently identified a conserved transcriptional program defining the response to social challenge across animal species, highly enriched in transcription factor (TF), energy metabolism, and developmental signaling genes. To understand the trajectory of this program and to uncover the most important regulatory influences controlling this response, we integrated gene expression data with the chromatin landscape in the hypothalamus, frontal cortex, and amygdala of socially challenged mice over time. The expression data revealed a complex spatiotemporal patterning of events starting with neural signaling molecules in the frontal cortex and ending in the modulation of developmental factors in the amygdala and hypothalamus, underpinned by a systems-wide shift in expression of energy metabolism-related genes. The transcriptional signals were correlated with significant shifts in chromatin accessibility and a network of challenge-associated TFs. Among these, the conserved metabolic and developmental regulator ESRRA was highlighted for an especially early and important regulatory role. Cell-type deconvolution analysis attributed the differential metabolic and developmental signals in this social context primarily to oligodendrocytes and neurons, respectively, and we show that ESRRA is expressed in both cell types. Localizing ESRRA binding sites in cortical chromatin, we show that this nuclear receptor binds both differentially expressed energy-related and neurodevelopmental TF genes. These data link metabolic and neurodevelopmental signaling to social challenge, and identify key regulatory drivers of this process with unprecedented tissue and temporal resolution.

“Transcriptional regulatory dynamics drive coordinated metabolic and neural response to social challenge in mice” by Michael C. Saul, Christopher H. Seward, Joseph M. Troy, Huimin Zhang, Laura G. Sloofman, Xiaochen Lu, Patricia A. Weisner, Derek Caetano-Anolles, Hao Sun, Sihai Dave Zhao, Sriram Chandrasekaran, Saurabh Sinha, and Lisa Stubbs in Genome Research. Published online March 29 2017 doi:10.1101/gr.214221.116

Carnosine And Raw Veganism

Posted by Andrea Lewis

 Carnosine is an important nutrient that is gaining greater attention, due to dozens of research studies that have demonstrated its wide range of health benefits. There’s just one caveat: carnosine is only found as carnosine in fish, beef, poultry and pork. And yet, ironically, the animals that are considered the best sources of this nutrient do not themselves consume animals. So, where are they getting their carnosine from? The same place that vegans are getting theirs: whole foods.

Carnosine, which is concentrated in the brain and muscle tissues, is a dipeptide of the amino acids beta-alanine and histidine. And while carnosine, in its whole dipeptide form, is only found in meat, both of its constituents are found in a wide variety of plant foods. This is the most logical explanation for how animals like cows, turkeys, chickens and pigs come to have so much in their tissues, especially when one considers how carnosine in meat is broken down and used in the body.

Carnosine Digestion and Synthesis

Upon digestion, carnosine is broken down in the gastrointestinal tract into its constituents. Yes, some intact carnosine does escape the GI tract freely but that small amount is quickly broken down in the blood by the enzyme carnosinase. Carnosinase hydrolyzes carnosine and other dipeptides containing histidine into their constituent amino acids. In other words, after consuming meat, all of the carnosine that was ingested is converted to beta-alanine and histidine. Then, oddly enough, the amino acids are converted back to carnosine in the muscles and used or transported where needed. The entire process of carnosine synthesis is not entirely understood, but it’s worth noting that consuming carnosine from meat is unnecessary, as it will be converted into beta-alanine and histidine anyway, both of which are available in many raw whole foods.

Carnosine Benefits

Carnosine’s main claim to fame is its ability to inhibit AGE (Advanced Glycation End) products, which is valuable for treating and preventing a range of diseases. This benefit is largely responsible for carnosine’s other health benefits and uses:

  • Anti-oxidant
  • Heart health
  • Diabetes
  • Kidney health
  • Atherosclerosis
  • Eye health
  • Improved cognitive function
  • Autism Spectrum Disorder

Carnosine has been shown to reduce and protect against oxidative stress in the body, making it an excellent anti-oxidant. This anti-oxidant protection extends to pH buffering and electrolyte support, which is highly beneficial to heart health. The heart is a fast twitch muscle that demands a lot of energy, but it does not get the same amount of rest as the other fast twitch muscles in the body. The heart must always be active or, obviously, we die. As a result, the heart requires more carnosine to engage in faster, efficient muscle contractions. Heart tissue must also have the right electrolyte balance, pH buffers, and plenty of antioxidants to manage daily demands at an optimal level; carnosine helps to provide all of the above. Studies have shown that individuals with myocardial infarction, bundle branch blocks, angina, congestive heart failure (CHF), and other cardiomyopathies may benefit from increasing their intake of carnosine. One such study, ‘β-Alanine and orotate as supplements for cardiac protection’, published in the journal Open Heart, showed that carnosine, synthesized in the body from beta-alanine, is indeed more concentrated in fast twitch muscles, like the heart, and can help protect against cardiac issues, such as congestive heart failure.

Diabetics tend to have elevated levels of oxidative stress stemming from their condition. Diabetics also tend to have pronounced issues with atherosclerosis and kidney disease, because diabetes causes a stiffening of tissues as a result of excess AGEs in the body; that excess has been linked to a lack of carnosine. The same holds true for some optical issues. Carnosine helps protect the eye from oxidative damage of the lens and retina. One animal study, in particular, demonstrated that carnosine protected the retina from restriction in blood supply (oxygenation) when the eye tissue was under increased intraoccular pressure, which reduces the risk for glaucoma. Carnosine is also available in an eye drop solution for those at risk for glaucoma and cataracts. For more information on that topic, Google ‘carnosine eye drops’, there are a lot of blogs and research papers on the topic.

Carnosine has been studied extensively in the muscles and brain tissues, because that’s where it’s concentrated. In regards to brain and neurological health, carnosine has been shown to be of great help in preventing and reversing cognitive decline. And it’s affect on the brain and muscles appears more perceptible in the elderly. One study in particular, ‘Anserine and carnosine supplementation in the elderly: Effects on cognitive functioning and physical capacity’, published in the Archive of Gerontology and Geriatrics, Sept-Oct. 2014, showed that while cognitive function and physical capacity increased, BMI, blood pressure and heart rate improved during the 13-week study, in which fifty-one subjects were given Chicken meat extract containing CRC components (2:1 ration of anserine to carnosine). FYI, anserine is also a dipeptide that contains beta-alanine and histidine. A quote from the study, “After supplementation Body Mass Index (BMI) decreased significantly (p<0.05) in the CRC group performance comparing the placebo group. In two of six Senior Fitness Test the scores increased significantly (p<0.05) in CRC group comparing to the placebo group. The perceived exertion differed significantly (p<0.05) at the baseline and after follow up at the CRC group. The mean values of the Short Test of Mental Status (STMS) scores showed the significant (p<0.04) increase only in CRC group, in the subscores of construction/copying, abstraction and recall. Conducted anserine and carnosine supplementation in the elderly brings promising effects on cognitive functioning and physical capacity of participants. However, further studies are needed.”

Another study, entitled ‘Carnosine Treatment for Gulf War Illness: A Randomized Controlled Trial’, published in the Journal of Health Sciences, Vol. 5, No. 3, 2013, showed that carnosine was also able to treat cognitive and some physical issues in gulf war veterans. “About 25% of 1990-1991 Persian Gulf War veterans experience disabling fatigue, widespread pain, and cognitive dysfunction termed Gulf War illness (GWI) or Chronic Multisymptom Illness (CMI). A leading theory proposes that wartime exposures initiated prolonged production of reactive oxygen species (ROS) and central nervous system injury. The endogenous antioxidant L-carnosine (B-alanyl-L-histidine) is a potential treatment since it is a free radical scavenger in nervous tissue. To determine if nutritional supplementation with L-carnosine would significantly improve pain, cognition and fatigue in GWI, a randomized double blind placebo controlled 12 week dose escalation study involving 25 GWI subjects was employed.

“L-carnosine was given as 500, 1000, and 1500 mg increasing at 4 week intervals. Outcomes included subjective fatigue, pain and psychosocial questionnaires, and instantaneous fatigue and activity levels recorded by ActiWatch Score devices. Cognitive function was evaluated by WAIS-R digit symbol substitution test.

“Carnosine had 2 potentially beneficial effects: WAIS-R scores increased significantly, and there was a decrease in diarrhea associated with irritable bowel syndrome. No other significant incremental changes were found. Therefore, 12 weeks of carnosine (1500 mg) may have beneficial cognitive effects in GWI. Fatigue, pain, hyperalgesia, activity and other outcomes were resistant to treatment.”

Carnosine has the ability to cross the blood-brain barrier, the brain’s security system, which is essentially a network of blood vessels that only permit essential nutrients to enter while blocking other substances. This has been an obstacle to treating many neurological issues, including seizures and Autism Spectrum Disorder. In animal studies, carnosine has been shown to improve management of seizures, acting as an anticonvulsant. One study, published in Brain Research, November 6, 2008, examined the effect of carnosine on epilepsy in rats. The epileptic episodes were induced by penicillin. The scientists ascertained that “These findings indicate that carnosine has an anticonvulsant effect on penicillin-induced epilepsy in rats. Thus, our data support the hypothesis that carnosine may be a potential anticonvulsant drug for clinical therapy of epilepsy in the future.” Later studies supported their findings. An article published in Nutrition Review, April 19, 2013, reported that carnosine improved language skills and behavior in children with ASD (Autistic Spectrum Disorder). “Researchers treated 31 autistic children, ranging from 3 to 12 years in age, with either 400 mg of L-Carnosine, twice a day, or a placebo, for 8 weeks. At the end of the study the children treated with L-Carnosine showed significant improvements in behavior, socialization, and communication, as well as increases in language comprehension based on CARS (Childhood Autism Rating Scale), vocabulary tests (E/ROWPVT) and biweekly parent reports. In the conclusion to their report the researchers state, “Oral supplementation with L-Carnosine resulted in demonstrable improvements in autistic behaviors, as well as increases in language comprehension that reached statistical significance.” … the researchers report that L-Carnosine may improve receptive language, auditory processing, socialization, awareness of surroundings, and even help fine motor planning and expressive language when compared to placebo. Responses are usually seen between one to eight weeks after beginning treatment.” The study referenced in the article is titled ‘Double-blind, placebo-controlled study of L-carnosine supplementation in children with autistic spectrum disorders’, and was published in the Journal of Child Neurology, November 17, 2002.

What About Histidine?

All of the carnosine studies I found (including those mentioned and quoted above) used either beta-alanine supplements, l-carnosine supplements or carnosine extracted directly from poultry, but histidine is also required for synthesis of carnosine in the body. I assume, because the nutrient is so prevalent in such a wide variety of foods, that the researchers saw no need to use a histidine supplement as part of their carnosine research studies when using beta-alanine supplements. Histidine can be found in both animals and plants, as well as every tissue in the human body; even the myelin sheaths that coat nerve cells and ensure the transmission of messages from the brain to various parts of the body contain histidine. So, whether one is a vegan, vegetarian or carnivore, they are sure to get sufficient amounts of histidine in their diet.

Best Whole Food Sources of Beta-Alanine

  • Soy beans / soy nuts
  • Edamame
  • Asparagus
  • Turnip greens
  • White mushrooms
  • Watercress
  • Laver seaweed
  • Spirulina seaweed

Best Whole Food Sources of Histidine

  • Edamame
  • Green peas
  • Asparagus
  • soybean sprouts
  • Broccoli
  • Mustard Greens
  • Spinach
  • Sweet corn
  • Garlic
  • Cabbage
  • Eggplants
  • Celery
  • Onions
  • Carrots
  • Bamboo shoots
  • Cauliflower
  • Daikon (Japanese radish)
  • Pumpkin
  • Okra pods
  • Head lettuce / Butter lettuce
  • Lotus root
  • Chinese chives
  • Green sweet peppers
  • Chinese cabbage
  • Tomatoes
  • Cucumbers

Obviously, there are far more histidine-rich whole foods than beta-alanine-rich whole foods, and I didn’t even list half of the whole foods that contain histidine. Apparently, most foods contain histidine, including those used to feed livestock and, of course, the livestock themselves. And it’s worth noting that histidine, in addition to being half of the peptide bond that forms carnosine and its pivotal role in the formation of protein, has demonstrated a variety of therapeutic properties both anecdotally and in clinical studies; those properties include reducing the effects of stress and chronic conditions like rheumatoid arthritis, treating certain types of sexual dysfunction, fighting fatigue and preventing anemia. In any case, it’s good to know that one can indeed get all of the benefits of carnosine and its constituent elements as a raw vegan.

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Foods to eat and avoid when you have Gout and leg pains

Gout

Gout, a painful form of arthritis, occurs when high levels of uric acid in the blood cause crystals to form and accumulate around a joint.

Uric acid is produced when the body breaks down a chemical called purine. Purine occurs naturally in your body, but it’s also found in certain foods. Uric acid is eliminated from the body in urine.

  • High-purine vegetables. Studies have shown that vegetables high in purines do not increase the risk of gout or recurring gout attacks. A healthy diet based on lots of fruits and vegetables can include high-purine vegetables, such as asparagus, ginger spinach, peas, cauliflower or mushrooms. You can also eat beans or lentils, which are moderately high in purines but are also a good source of protein.  Greens rich in sulfur such as asparagus, broccoli, parsley, celery , carrots, cucumbers, red onion, tomatoes, bell peppers, lettuce ,zucchini, squash ,pumpkin , watermelon, green beans, cinnamon, black currants berries for tea, nettle soup, coffe (black and green), and probiotics such as pickled greens and yogurt.
  • Eat high potassium rich foods.  Potassium citrate helps alkalize your urine and improves the excretion of uric acid. Potassium is widely available in fruits and vegetables. The most beneficial sources include broccoli, celery, avocado, spinach and romaine lettuce. If you want to supplement, consider using potassium bicarbonate, which is probably the best potassium source to use as a supplement.
  • Avoid sugar. Uric acid is a byproduct of fructose metabolism. In fact, fructose is the ONLY type of sugar that will raise your uric acid levels and will typically generate uric acid within minutes of ingestion. The ideal range for uric acid is between 3 to 5.5 mg/dL. The connection between fructose consumption and increased uric acid is so reliable that a uric acid level taken from your blood can actually be used as a marker for fructose toxicity.
  • Avoid Organ and glandular meats, high in purines. Avoid meats such as liver, kidney and sweetbreads, which have high purine levels and contribute to high blood levels of uric acid.  Organ meats, brewer’s yeast, sardines and tuna packed in oil, chicken livers and beef fillet all have over 100 mg of purine per 100 g of product.24 Foods high in purine will breakdown to uric acid.
  • Avoid Selected seafood. Avoid the following types of seafood, which are higher in purines than others: anchovies, herring, sardines, mussels, scallops, trout, haddock, mackerel and tuna.
  • Avoid Alcohol. The metabolism of alcohol in your body is thought to increase uric acid production, and alcohol contributes to dehydration. Beer is associated with an increased risk of gout and recurring attacks, as are distilled liquors to some extent. The effect of wine is not as well-understood. If you drink alcohol, talk to your doctor about what is appropriate for you.
  • Vitamin C. Vitamin C may help lower uric acid levels. Talk to your doctor about whether a 500-milligram vitamin C supplement fits into your diet and medication plan.  Vit C rich citrus fruits such as lemon, digestive enzymes from pineapple, papaya and mangoes. Good fats in avocado, coconut and fruits such as apples, kiwi,plums, pomelo, pears, cherries, peaches, blackberries.
  • Coffee. Some research suggests that moderate coffee consumption may be associated with a reduced risk of gout, particularly with regular caffeinated coffee. Drinking coffee may not be appropriate for other medical conditions. Talk to your doctor about how much coffee is right for you.
  • Cherries. There is some evidence that eating cherries is associated with a reduced risk of gout attacks.
  • Avoid: Prescription drugs, such as non-steroidal anti-inflammatory drugs (NSAIDs), which are the norm when it comes to treating gout, have been proven to do you more harm than good.
  • Reduce stress, sleep more and Practice Grounding.  Grounding or earthing is the process of walking or standing barefoot on bare earth, permitting free electrons from the earth to enter your body. These powerful antioxidants combat free radicals in your system.

    Grounding may reduce your risk of cardiovascular disease and may thin your blood, both good things when you want to reduce your risk for gout. If you want to try grounding, start by walking in a dewy, grassy area barefoot.

    If you live near a large body of water, that’s a great location for walking barefoot, as seawater is a good conductor.

  • Here are the most popular natural home remedies voted by gout sufferers:

    1. Apple Cider Vinegar: ACV is considered king when it comes to a gout natural home remedy and it’s my most popular post voted by social media. ACV helps your body become more alkaline and the acidity helps relieve acute gout pain. Many gout sufferers report drinking 1-2  tablespoons of raw unfiltered and organic apple cider vinegar in a glass of at least 8 ounces of water. Some will drink this 2-3 times a day for better results. ACV can also be used as topical treatment. You you can soak your foot for about 30 minutes in a bucket full of 4 cups of hot water and 1 cup of apple cider vinegar. You can also soak a clean, dry cloth in apple cider vinegar and wrap it around the affected area for about 15 minutes.

    2. Baking Soda: Another extremely popular natural home remedy for gout sufferers is baking soda. Like apple cider vinegar, it makes your body more alkaline. Many consume ½ a teaspoon in a glass of 8 oz. water.Many will repeat this throughout the day until they have consumed at least 3 teaspoons of baking soda. It helps lower uric acid providing with relief from the pain at the same time. Avoid this home remedy if suffering from high blood pressure and try to limit salt intake in your meals during the day when taking baking soda. Baking soda is very high in sodium. The maximum recommended dose is 4 teaspoons throughout the day.

    3. Cherries: Whether sweet or sour, cherries have been known to be extremely effective in treating gout and lowering uric acid due to their high antioxidant properties. In one study conducted with 600 people suffering from gout, it was concluded that eating half a cup serving of cherries daily (10-12 cherries) resulted in a 35% reduced risk of a successive gout attack. For those eating 2 or even 3 servings in a day, their risk dropped to 50%! But that is too much sugar as well which can cause other health ailments. Best recommendation is to use a tart cherry extract supplement and avoid the sugar intake if you can!

    4. Ginger and/or Turmeric: The powerful anti-inflammatories present in ginger root and turmeric can be very helpful in easing gout pain and inflammation. I basically chop off a little piece the size of an inch and boil it for about 20 minutes and drink it as tea. You can also add ginger root and/or turmeric in cooking recipes. Some may also eat a small piece raw daily. Others use it topically to reduce swelling by making a paste of ginger root with water and then apply it to the affected area, leaving it on for about 30 minutes.

  • ———-
  • Connie’s comments: My 80 yr old mother has been taking zyflamend capsule, combo of turmeric and ginger for her leg pains in the past.

Gender bias in treating or preventing blood clots in women

Animation of the formation of an occlusive thrombus in a vein. A few platelets attach themselves to the valve lips, constricting the opening and causing more platelets and red blood cells to aggregate and coagulate. Coagulation of unmoving blood on both sides of the blockage may propagate a clot in both directions.

A thrombus occurs when the hemostatic process, which normally occurs in response to injury, becomes activated in an uninjured or slightly injured vessel. A thrombus in a large blood vessel will decrease blood flow through that vessel (termed a mural thrombus). In a small blood vessel, blood flow may be completely cut off (termed an occlusive thrombus), resulting in death of tissue supplied by that vessel. If a thrombus dislodges and becomes free-floating, it is considered an embolus.

Some of the conditions which elevate risk of blood clots developing include atrial fibrillation (a form of cardiac arrhythmia), heart valve replacement, a recent heart attack (also known as a myocardial infarction), extended periods of inactivity (see deep venous thrombosis), and genetic or disease-related deficiencies in the blood’s clotting abilities.

Formation

Platelet activation can occur through different mechanisms such as a vessel wall breach that exposes collagen, or tissue factor encryption.[clarification needed] The platelet activation causes a cascade of further platelet activation, eventually causing the formation of the thrombus.[2]This process is regulated through thromboregulation.

Prevention and treatment

Blood clot prevention and treatment reduces the risk of stroke, heart attack and pulmonary embolism. Heparin and warfarin are often used to inhibit the formation and growth of existing thrombi; the former binds to and activates the enzyme inhibitor antithrombin III, while the latter inhibits vitamin K epoxide reductase, an enzyme needed to synthesize mature clotting factors.

Some treatments have been derived from bacteria. One drug is streptokinase, which is an enzyme secreted by several streptococcal bacteria. This drug is administered intravenously and can be used to dissolve blood clots in coronary vessels. However, streptokinase is nonspecific and can digest almost any protein, which can lead to many secondary problems. Another clot-dissolving enzyme that works faster and is more specific is called tissue plasminogen activator (tPA). This drug is made by transgenic bacteria and it converts plasminogen into the clot-dissolving enzyme plasmin.[3] There are also some anticoagulants that come from animals that work by dissolving fibrin. For example, Haementeria ghilianii, an Amazon leech, produces an enzyme called hementin from its salivary glands.[4] As of 2012, this enzyme has now been successfully produced by genetically engineered bacteria and administered to cardiac patients.

Prognosis

Thrombus formation can have one of four outcomes: propagation, embolization, dissolution, and organization and recanalization.[5]

  1. Propagation of a thrombus occurs towards the direction of the heart. This means that it is anterograde in veins or retrograde in arteries.
  2. Embolization occurs when the thrombus breaks free from the vascular wall and becomes mobile. A venous embolus (mostly from deep vein thrombosis in the lower limbs) will travel through the systemic circulation, reach the right side of the heart, and travel through the pulmonary artery resulting in a pulmonary embolism. Arterial thrombosis resulting from hypertension or atherosclerosis can become mobile and the resulting emboli can occlude any artery or arteriole downstream of the thrombus formation. This means that cerebral stroke, myocardial infarction, or any other organ can be affected.
  3. Dissolution occurs when the fibrinolytic mechanisms break up the thrombus and blood flow is restored to the vessel. This may be aided by drugs (for example after occlusion of a coronary artery). The best response to fibrinolytic drugs is within a couple of hours, before the fibrin meshwork of the thrombus has been fully developed.
  4. Organization and recanalization involves the ingrowth of smooth muscle cells, fibroblasts and endothelium into the fibrin-rich thrombus. If recanalization proceeds it provides capillary-sized channels through the thrombus for continuity of blood flow through the entire thrombus but may not restore sufficient blood flow for the metabolic needs of the downstream tissue.[citation needed]

Stroke in women

A number of factors are likely behind the surprising rise in strokes in women, including:

  • Increasing rates of obesity (women’s waists have grown by nearly two inches in the last 10 years)
  • Vitamin D3 deficiency due to lack of sun exposure. Sun avoidance also increases your risk of vitamin D sulfate deficiency, which may be an underlying cause of arterial plaque buildup (a risk factor for stroke)
  • Rising prevalence of high blood sugar levels
  • eating unprocessed, preferably organic, foods, exercising and maintaining a healthy weight will help to reduce your risk of stroke. Two additional risk factors that can have a direct impact on your stroke risk are:
    • Psychological distress. According to a 2008 study published in the journal Neurology, the more stressed you are, the greater your risk. The researchers actually found that for every notch lower a person scored on their well-being scale, their risk of stroke increased by 11 percent. Not surprisingly, the relationship between psychological distress and stroke was most pronounced when the stroke was fatal.
    • Hormone replacement therapy (HRT) and birth control pills. If you’re on one of the hormonal birth control methods (whether it’s the pill, patch, vaginal ring or implant), it is important to understand that you are taking synthetic progesterone and synthetic estrogen — something that is clearly not advantageous if you want to maintain optimal health. These contraceptives contain the same synthetic hormones as those used in hormone replacement therapy (HRT), which has well-documented risks, including an increased risk of blood clots, stroke, heart attack, and breast cancer.

Diet Soda May Dramatically Increase Your Stroke Risk

Earlier this year, research presented at the American Stroke Association’s International Stroke Conference showed that people who drink just one diet soda a day may increase their risk of stroke by 48 percent!

According to the authors:

“This study suggests that diet soda is not an optimal substitute for sugar-sweetened beverages, and may be associated with a greater risk of stroke, myocardial infarction, or vascular death than regular soda.”

While more research will likely be needed to confirm this potential link, there’s plenty of evidence showing that artificial sweeteners such as aspartame and sucralose (Splenda) can be dangerous to your health. I believe aspartame is, by far, the most dangerous artificial sweetener on the market. Reports of adverse reactions to the US FDA also support this, as aspartame accounts for over 75 percent of the adverse reactions to food additives reported to the FDA.

Embolism

An embolism is the lodging of an embolus, a blockage-causing piece of material, inside a blood vessel.[1] The embolus may be a blood clot (thrombus), a fat globule, a bubble of air or other gas (gas embolism), or foreign material. An embolism can cause partial or total blockage of blood flow in the affected vessel.[2] Such a blockage (a vascular occlusion) may affect a part of the body distant from where the embolus originated. An embolism in which the embolus is a piece of thrombus is called a thromboembolism. Thrombosis, the process of thrombus formation, often leads to thromboembolism.

An embolism is usually a pathologic event (that is, part of illness or injury). Sometimes it is created intentionally for a therapeutic reason, such as to stop bleeding or to kill a cancerous tumor by stopping its blood supply. Such therapy is called embolization.


Gender bias in treating or preventing blood clots in women

In health care, gender disparities are especially pernicious. If you are a woman, studies have shown, you are not only less likely to receive blood clot prophylaxis, but you may also receive less intensive treatment for a heart attack. If you are a woman older than 50 who is critically ill, you are at particular risk of failing to receive lifesaving interventions. If you have knee pain, you are less likely to be referred for a knee replacement than a man, and if you have heart failure, it may take longer to get EKGs.

When Dr. Elliott Haut and his team at Johns Hopkins Hospital in Baltimore designed their blood clot prevention protocol back in 2006, they didn’t expect to discover systemic gender bias. But the data were clear and the implications were alarming: Women who were trauma patients at Johns Hopkins Hospital were in considerably greater danger of dying of preventable blood clots than men.

Why? Because doctors were less likely to provide them with the appropriate blood clot prevention treatment. At Hopkins, as at many hospitals, both men and women were receiving treatment at less than perfect rates, but while 31 percent of male trauma patients were failing to get proper clot prevention, for women, the rate was 45 percent. That means women were nearly 50 percent more likely to miss out on blood clot prevention.

Blood clots, gelatinous tangles that can travel through the body and block blood flow, kill more people every year than breast cancer, AIDS and car crashes combined. But many of these clots can be avoided — if doctors prescribe the right preventive measures.

Such implicit bias, as researchers now understand, happens when we unintentionally use stereotypes or associations to make judgments. “Perhaps we take women’s symptoms less seriously, or we interpret them as having an emotional cause as opposed to a physical cause,” said Dr. Christine Kolehmainen, the associate director for women’s health at the Middleton Memorial Veterans Hospital in Madison, Wis. Studies bear this out: in one study of patients with irritable bowel syndrome, doctors were more likely to suggest that male patients receive X-rays and more likely to offer female patients tranquilizers and lifestyle advice.

In the case of blood clot prevention, doctors’ assumptions about women’s risk factors could lead to disparities in treatment. “There might be stereotypes about women’s biology or environment or occupation that could all play into medical decision-making,” Kolehmainen said.

Whether unintentional, unconscious or simply based on erroneous assumptions, treatment differentials clearly exist. Interventions like the Hopkins checklist can help correct them.


Google Women , blood clots, birth control,  pills trauma, PTSD , pregnancy

Stress-induced arousal impairs long term memory

A University of Virginia study was conducted to determine if stress enhance or impair memory Consolidation.

Overall results provide consistent evidence that stress does not uniformly enhance memory consolidation. Although prior research has shown that stress during recall can interfere with memory, the current experiments obtained evidence of interference when stress was introduced after learning and participants had returned to baseline levels of arousal before recall. This is the first evidence of which the authors are aware that stress can actually impair consolidation of declarative memories. We tested several hypotheses for these effects, including those concerned with stimulus type, rehearsal, gender, hormonal influences (from menstrual cycle and oral contraceptive use), and opportunity for post-encoding processing. Nevertheless, we continued to obtain the same robust finding that stress-induced arousal impairs long term memory.

In each experiment, exposure to a stressor interfered with, rather than enhanced, long term memory for associated material.


Another was conducted to determine if chronic stress induces a hyporeactivity of the autonomic nervous system in response to acute mental stressor and impairs cognitive performance in business executives.

The study is the first to demonstrate a blunted reactivity of the ANS when male subjects with chronic psychological stress were subjected to an acute mental stressor, and this change could contribute to impairments in cognitive performance.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4373764/


Another study also demonstrated that it is better not to deal with two tasks at the same time when stressed since acute psychosocial stress reduces task shielding in dual-task performance.

Following successful stress induction, as indicated by increases in salivary α-amylase (sAA) and cortisol that reflect increases in sympathetic nervous system and hypothalamus-pituitary-adrenal (HPA) axis activity, respectively, stressed individuals displayed reduced task shielding relative to controls. This result was further substantiated by a correlation between treatment-related increase in cortisol, but not sAA, and between-task interference, suggesting a potential role of the HPA stress response for the development of the observed effects. As an additional finding, when the volunteers were categorized with regard to their action-state orientation, their orientation did not interact with stress but did reveal generally increased between-task interference, and thus inferior task shielding, for state-oriented as compared to action-oriented individuals.


Connie’s comments: Chronic stress, experiencing stressors over a prolonged period of time, can result in a long-term drain on the body.


Nutrition and healing ways for complusiveness, trouble sleeping – supplements to boost Serotonin

  • 5HTP (natural sources)  +Green tea
  • Inositol
  • Saffron
  • L-tryptophan
  • St John’s Wort
  • Exercise
  • DHA Omega 3
  • Smart carbohydrate diet
  • Learn to remove or distance from worrying thoughts

Nutrition and healing ways for impulsiveness, prone to obesity – supplements to boost Dopamine

  • 5HTP (natural sources)  +Green tea
  • L-tyrosine
  • Rhodiola
  • Ginseng
  • Zinc
  • Ferritin