(Isabelle Z.) Fluoride is everywhere these days. Perhaps you’re one of the 200 million Americans whose municipal water contains this neurotoxin, or maybe you’re worried about exposure via toothpaste. Sodium fluoride accumulates in the body and the brain, and high levels can bring about neurological damage. It might seem like there isn’t much you can do about it, but the fruit of one tree might be able to save the day: tamarind.
This tropical evergreen tree is native to Africa, but it can now be found in places like Mexico, Australia, and South Asia. Pod-like fruits grow from these tall trees and, as they mature, they go from green and sour to brown and juicy with a sweet-and-sour pulp. It’s used in Indian cooking and also popular as a folk remedy.
The flavor of the fruit might not be to everyone’s liking, but its benefits can make it far more appealing. A study that was published in the European Journal of Clinical Nutrition showed that it can remove risky fluoride deposits from your bones. In the study, researchers discovered that healthy boys who consumed a third of an ounce of the fruit for just 18 days noted significant enhancements in their urinary excretion of fluoride. In another study, boys who were given tamarind to eat for just three weeks noted additional fluoride excretion compared to a control group.
That is good news for anyone who is concerned about the effects of fluoride, which are numerous and downright disturbing. It has been linked to everything from several types of cancer and reduced IQ to infertility, low thyroid function, and a debilitating bone disease.
However, tamarind also provides another incredibly useful benefit: It can prevent and alleviate chronic diseases. Tamarind seed extract has been shown to target and kill inflammatory chemicals like interleukin, reducing joint pain, swelling and inflammation. This makes it quite useful or those who suffer from osteoarthritis.
In addition, its rich vitamin C content means it can boost immunity and help detoxify. It’s a good source of potassium, supporting healthy blood pressure, and it also helps prevent heart disease by removing excess LDL cholesterol from the veins and arteries in the body. It also promotes circulation and normalizes the levels of triglycerides in the blood. In addition, it boasts a significant iron content, helping to ward off anemia.
It can even be useful in the fight against obesity. Consuming it raises levels of the neurotransmitter serotonin, which controls weight as well as appetite. At the same time, its high fiber content helps curb out-of-control appetites and promotes digestion.
How can you get the benefits of tamarind?
If you have access to fresh tamarind, you can simply eat the fruit as it is. Be sure to seek the organic varieties. It can also be bought in slices, blocks, concentrate, or paste. In addition, you can buy the dried seed pods, which should be cracked open and boiled. If you go this route, the inner pulp should be dark brown, and the fruit should not smell bitter.
It’s important to note, however, that tamarind can thin your blood, so be careful if you take aspirin or other blood-thinning medications.
According to the Fluoride Action Network, many children now exceed the recommended daily fluoride intake just by using toothpaste. More than 50 studies have linked fluoride to lower IQ in children. If you are worried about fluoride exposure for you and your loved ones, tamarind could prove to be an essential part of your diet.
Over the past six months, I have engaged in a simple experiment. In packed rooms in Europe and the United States, I have asked, “What is your favorite African dish?”
Usually, the answer is blank stares.
In contrast, when I’ve asked, “What is your favorite Asian dish?” the list from the audience has been long, often including sushi, pad thai and samosas.
I also gauged the audience’s recognition of Africa’s role in the global food industry, asking about commodities such as cocoa, cashews, yam, coffee and tea, to more niche products such as rooibos, moringa or fonio. Typically, awareness has been extremely low—everyone loves chocolate, but most do not realize that 70% of the world’s cocoa is sourced from West Africa or that rooibos tea is grown in the hills of South Africa.
My informal polling tallies with the sparse survey results on global preferences for food which often excludes food from African countries, or gives the entire continent the lowest ratings—categorized as one type of food, instead of the diversity of 54 countries. Sadly, this global perception is seeping into the continent as well, with young Africans opting for fast food from international chains like KFC, Dominos and even Krispy Creme, which are making significant inroads into major African cities.
What this means is the world is missing out on the extremely diverse cuisine from across Africa, which is also highly nutritious. More importantly, it means we are limiting opportunities to foster greater global awareness about the culture and rich heritage of countries in Africa, and to promote cross-cultural learning.
These various findings, coupled with my personal investment in the transformation of the African agricultural and food landscapes over more than two decades have led me down a research path to discover how to change the disparity in the global appreciation and acceptance of African food.
Primarily, it will require African entrepreneurs to invest in branding and storytelling, innovation, and partnerships to accelerate broad-based awareness of African food. In addition, African governments must create an enabling environment and foster linkages with diaspora populations to attract the support required to position our food and change mindsets.
The rise of Japanese cuisine on the global stage offers compelling lessons for stakeholders in African countries.
The rise of Japanese cuisine on the global stage offers compelling lessons for committed stakeholders in key African countries. As is the case with Ethiopian, Senegalese or Nigerian cuisine today, in the 1960s and 70s, awareness and appreciation for Japanese food was limited overseas. Then the Japanese government took action after recognizing the important role food could play in building cultural bridges while also generating employment and demand for its food. In 2003, the Japanese government expanded the scope of the Japanese External Trade Organization (JETRO) to include branding, certification of restaurants and ingredients, and public relations. In addition, through strategic and deliberate interventions by the government, Japanese traditional cuisine was added to the UNESCO Intangible Cultural Heritage List in 2012.
The results of these efforts are very compelling. In 2006, there was approximately 20,000 Japanese restaurants outside Japan. By 2017, this number had increased five-fold to close to 120,000. Beyond the growth in restaurants, today, most leading supermarkets in the United States and the UK sell sushi. In addition, Japanese food attracts the highest ratings in foreign food preferences.
This rapid rise of Japanese food in the global food landscape demonstrates what is possible, through strategic and coordinated efforts from key stakeholders in the private and public sectors, and what can be replicated by Cote d’Ivoire, Ethiopia, Nigeria, and Senegal, which have unique cuisines across the different ethnic groups and regions, with distinct flavors.
Ethiopian cuisine already has a head-start as there are over 350 restaurants in the United States, driven by the immigration trends in the 1980s. Like Japanese food, Ethiopian food is considered extremely healthy. The Injera made of teff, is gluten-free, high in fiber, calcium, iron and protein, which also makes it very appealing to the growing global vegetarian and vegan community. This cuisine has the potential to gain widespread acceptance.
The momentum for food from other African countries is also building, with the emergence of celebrity chefs opening high-end restaurants in global cities. Senegalese chef Pierre Thiam, for instance, through his restaurant Teranga in New York City, and his company—Yolélé Foods, is committed to sharing African culture through food, and promoting fonio as an attractive substitute to quinoa. Kwame Onwuachi a second-generation Nigerian-American chef based in Washington DC, was just named on the TIME 100 List. Now is the time to build on this momentum and ensure that varied, healthy and tasty African dishes are promoted globally.
Greater global awareness and appreciation for African food will require key stakeholders in international markets open their minds and pallets to food from African countries. For example, high schools and universities could add healthy options from the African Continent to their menus, introducing children and youth to new culinary experiences. Trade officials would also need to ease trade barriers for food imports from African countries and partner with regulators to enhance the capacity of entrepreneurs to meet global standards.
Indeed, repositioning African food globally will not only increase the demand for food sourced from African farmers, and create jobs for Africans locally and globally, but it will also build more bridges between Africa and the rest of the world, breaking stereotypes and biases and ultimately enabling a deeper appreciation of our connections as humans.
Irish moss is Irish moss, sea moss is sea moss! After soaking the moss in part one, it’s now time to boil it up and get ready to make some JUICE. We chat rasta hand oven mitts, whistling frogs VS rasclaat toads, Sea Moss Vs Irish Moss facts, checking out ponganut aka pomegranate baby trees with ratty, dealing with ant and mosquito bites, and also g into a pot lid toe mashup accident xD Part 2 with taste test coming soon 😉 Bless up, Matthew & Mokko
The company’s protein powder, “Solein,” is similar in form and taste to wheat flour.
Based on a concept developed by NASA, the product has wide potential as a carbon-neutral source of protein.
The man-made “meat” industry just got even more interesting.
It’s not like you can make food out of thin air. Well…it turns out you can. A company from Finland, Solar Foods, is planning to bring to market a new protein powder, Solein, made out of CO₂, water and electricity. It’s a high-protein, flour-like ingredient that contains 50 percent protein content, 5–10 percent fat, and 20–25 percent carbs. It reportedly looks and tastes like wheat flour, and could become an ingredient in a wide variety of food products after its initial launch in 2021.
It’s likely to first appear on grocery shelves in protein shakes and yogurt. It could be an exciting development: Solein’s manufacturing process is carbon neutral and the potential for scalability seems unlimited — we’ve got too much CO₂, if anything. Why not get rid of some greenhouse gas with a side of fries?
Image source: Solar Foods
Solar Foods makes Solein by extracting CO₂ from air using carbon-capture technology, and then combines it with water, nutrients and vitamins, using 100 percent renewable solar energy from partner Fortum to promote a natural fermentation process similar to the one that produces yeast and lactic acid bacteria.
When the company claims its single-celled protein is “free from agricultural limitations,” they’re not kidding. Being produced indoors means Solar Foods is not dependent on arable land, water (i.e., rain), or favorable weather.
The company is already working with the European Space Agency to develop foods for off-planet production and consumption. (The idea for Solein actually began at NASA.) They also see potential in bringing protein production to areas whose climate or ground conditions make conventional agriculture impossible.
And let’s not forget all those beef-free burgers based on pea and soy proteins currently gaining popularity. The environmental challenge of scaling up the supply of those plants to meet their high demand may provide an opening for the completely renewable Solein — the company could provide companies that produce animal-free “meats,” such as Beyond Meat and Impossible Foods, a way to further reduce their environmental impact.
The larger promise
Image source: Solar Foods
The impact of the beef — and for that matter, poultry, pork, and fish — industries on our planet is widely recognized as one of the main drivers behind climate change, pollution, habitat loss, and antibiotic-resistant illness. From the cutting down of rainforests for cattle-grazing land, to runoff from factory farming of livestock and plants, to the disruption of the marine food chain, to the overuse of antibiotics in food animals, it’s been disastrous.
The advent of a promising source of protein derived from two of the most renewable things we have, CO₂ and sunlight, gets us out of the planet-destruction business at the same time as it offers the promise of a stable, long-term solution to one of the world’s most fundamental nutritional needs.
While company plans are always moderated by unforeseen events — including the availability of sufficient funding — Solar Foods plans a global commercial rollout for Solein in 2021 and to be producing two million meals annually, with a revenue of $800 million to $1.2 billion by 2023. By 2050, they hope to be providing sustenance to 9 billion people as part of a $500 billion protein market.
The project began in 2018, and this year, they anticipate achieving three things: Launching Solein (check), beginning the approval process certifying its safety as a Novel Food in the EU, and publishing plans for a 1,000-metric ton-per-year factory capable of producing 500 million meals annually.
The protein powder Solein. Image source: SOLAR FOODS
AFTER decades of disappointment, we may have a new lead on fighting Alzheimer’s disease. Compelling evidence that the condition is caused by a bacterium involved in gum disease could prove a game-changer in tackling one of medicine’s biggest mysteries, and lead to effective treatments or even a vaccine.
As populations have aged, dementia has skyrocketed to become the fifth biggest cause of death worldwide. Alzheimer’s constitutes some 70 per cent of these cases (see “What is Alzheimer’s disease”), yet we don’t know what causes it. The condition, which results in progressive loss of memory and cognitive function, usually over a decade or so, is devastating both to those who have it and to their loved ones.
The condition often involves the accumulation of two types of proteins – called amyloid and tau – in the brain. As these are among the earliest physical signs of the disease, the leading hypothesis since 1984 has been that the condition is caused by the defective control of these proteins, especially amyloid, which accumulates to form large, sticky plaques in the brain.
The bulk of research into understanding and treating Alzheimer’s has centred on this “amyloid hypothesis”. Huge sums of money have been invested in experiments involving mice genetically modified to produce amyloid, and in developing drugs that block or destroy amyloid proteins, or sometimes degraded tangles of tau.
It has become clear that this approach isn’t working. In 2018 alone, the US National Institutes of Health spent $1.9 billion on Alzheimer’s research. But according to a recent study, the failure rate of drug development for Alzheimer’s has been 99 per cent.
Some have begun to question the amyloid hypothesis. The lack of results has been compounded by the discovery that people – including some in their 90s with exceptional memories – can have brain plaques and tangles without having dementia. In a review of the research to date last year, Bryce Vissel at the University of Technology Sydney, Australia, concluded that there isn’t sufficient data to suggest that “amyloid has a central or unique role in Alzheimer’s”.
“The bacteria in the brain are not the result of Alzheimer’s, but they could be the cause”
In 2016, researchers discovered that amyloid seems to function as a sticky defence against bacteria. They found that the protein can act as an anti-microbial compound that kills bacteria, and when they injected bacteria into the brains of mice engineered to make Alzheimer’s proteins, plaques developed round bacterial cells overnight.
At the time, the team said it still believed that amyloid itself went on to cause the brain damage of Alzheimer’s, not bacteria. But a spate of subsequent studies have looked at microbes. Bacteria have been found in the brains of people who had Alzheimer’s when they were alive. But it hasn’t been clear whether the bacteria caused the disease or were simply able to enter brains damaged by Alzheimer’s.
“When science converges from multiple independent laboratories like this, it is very compelling,” says Casey Lynch of Cortexyme, a pharmaceutical firm in San Francisco.
Now researchers from Cortexyme and several universities have reported finding the two toxic enzymes that P. gingivalis uses to feed on human tissue in 99 and 96 per cent of 54 human Alzheimer’s brain samples taken from the hippocampus – a brain area important for memory (Science Advances, doi.org/gftvdt). These protein-degrading enzymes are called gingipains, and they were found in higher levels in brain tissue that also had more tau fragments and thus more cognitive decline.
The team also found genetic material from P. gingivalis in the cerebral cortex – a region involved in conceptual thinking – in all three Alzheimer’s brains they looked for it in.
“This is the first report showing P. gingivalis DNA in human brains, and the associated gingipains co-localising with plaques,” says Sim Singhrao at the University of Central Lancashire, UK, who wasn’t involved in the study. Her team has previously found that P. gingivalisactively invades the brains of mice with gum infections.
When Lynch and her colleagues looked at brain samples from people without Alzheimer’s, they saw that some had P. gingivalis and protein accumulations, but at low levels. We already know that amyloid and tau can accumulate in the brain for 10 or 20 years before Alzheimer’s symptoms begin. This, says the team, shows that P. gingivalis doesn’t get into the brain as a result of Alzheimer’s – but could be the cause.
When the team gave P. gingivalis gum disease to mice, it led to brain infection, amyloid production, tangles of tau protein and neural damage in the regions and nerves normally affected by Alzheimer’s. This suggests causation, says Lynch.
She adds that P. gingivalis fulfils an updated set of criteria for attributing a disease to a particular pathogen. These conditions are named Koch’s postulates, after Robert Koch, a founder of the germ theory of disease.
“The study does address most of Koch’s postulates,” says Robert Genco of the University at Buffalo, New York. “Future studies need to be in humans to be convincing.”
We don’t know how P. gingivalis gets into the brain, but there are plausible routes it could take. Your mouth normally hosts a diverse and relatively stable community of bacteria, but when dental plaque builds under the edge of your gums, it can form inflamed pockets in which P. gingivalis can thrive and release toxins.
This inflammation can lead to chronic periodontitis and tooth loss, and some studies have shown that people with fewer teeth are more likely to have dementia. The inflammation and toxins caused by P. gingivalis damage the lining of your mouth, which may make it possible for oral bacteria to enter the bloodstream and then other organs. Even if you don’t have gum disease, transient damage to your mouth lining from eating or tooth-brushing can let mouth bacteria into your blood, says Lynch.
The blood-brain barrier should protect your brain from microbes, but P. gingivalis can invade white blood cells and the cells lining blood vessels, so might cross it that way. It may also invade cranial nerves near the mouth, then spread from cell to cell towards the brain over a period of years.
“This is why years of efforts to treat Alzheimer’s have seen few results”
As to how P. gingivalis might cause dementia after it arrives in the brain, there are two clear possibilities. It may trigger the release of amyloid, the brain’s method of trying to contain the infection, and this may then kill neurons.
Or P. gingivalis may directly damage the brain. We already know that Alzheimer’s involves inflammation, an excessive immune response that ends up killing neurons instead of protecting them. P. gingivalis is known to cause inflammation in gum tissue, and it may do so in the brain as well.
In response to the new findings, David Reynolds of the Alzheimer’s UK charity said he is dubious that P. gingivalis causes Alzheimer’s, because of the evidence showing that a person’s genes play a crucial role in the disease. “Strong genetic evidence indicates that factors other than bacterial infections are central to the development of Alzheimer’s, so these new findings need to be taken in the context of this existing research,” he said in a statement.
But a bacterial hypothesis for Alzheimer’s doesn’t conflict with genetic evidence. The human body’s propensity for inflammation can vary according to genetic variations that affect our immune systems, and this may influence how much damage P. gingivalis induces in a brain.
The biggest genetic risk factor for Alzheimer’s is a variant of the gene that makes the ApoE immune protein. Last year, a team in Sweden found that the gingipains released by P. gingivalis break up the ApoE protein into fragments, cleaving it at the site of a particular amino acid within the protein, and that these fragments may harm nerves. The ApoE4 variant of this protein contains more of this amino acid, suggesting that the reason people who make this variant are at a higher risk of developing Alzheimer’s may be because harmful levels of ApoE protein fragments build up more quickly in their brains than in those of other people.
Hope for treatments
The speed at which damage accumulates is a key factor in the disease. Although many people harbour P. gingivalis in their mouths, only some develop Alzheimer’s. Because it can be decades before Alzheimer’s symptoms appear, whether a person develops the condition could come down to how much damage occurs before they die of other causes.
“Alzheimer’s strikes people who accumulate gingipains and damage in the brain fast enough to develop symptoms during their lifetimes,” says Lynch. She says her team’s findings are a “universal hypothesis of pathogenesis”, fully explaining the causes of Alzheimer’s disease.
But Vissel warns that Alzheimer’s is a complex disease. “The answer is unlikely to be one-cause-fits-all. We need to keep open eyes.”
However, the new study is “very exciting”, he says. “Alzheimer’s is so common in people at advanced age that I think it can only be either some intrinsic property of the brain, or an infection.”
If this new hypothesis of Alzheimer’s is borne out, the good news is that it could lead to effective treatments for the condition. Although there is plenty you can do to reduce your risk of gum disease, Cortexyme is hoping it can stop or even reverse Alzheimer’s using molecules it has developed that block gingipains. The firm found that giving some of these to mice with P. gingivalis infections reduced brain infection, halted amyloid production, lowered brain inflammation and even rescued damaged neurons. “This provides hope of treating or preventing Alzheimer’s disease one day,” says Singhrao.
Cortexyme reported last year that the best of its gingipain blockers had passed initial safety tests in people, and entered the brain. It also seemed to improve symptoms in participants with Alzheimer’s. The firm will launch a larger trial later this year.
The company also plans to test the drug against gum disease itself. Efforts to fight that have led a team in Melbourne to develop a vaccine for P. gingivalis that started tests in 2018. A vaccine for gum disease would be welcome – and if it also stops Alzheimer’s the impact could be enormous.
It is early days for this new hypothesis, and if the pursuit of amyloid-busting drugs over the past few decades has taught us anything, says Vissel, it is that a complex disease may not have a simple mechanism. Even if P. gingivalis is confirmed as a cause of Alzheimer’s, we don’t know yet whether it will turn out to be the only cause or one of several factors contributing to the disease.
“This paper is very important,” says George Perry at the University of Texas at San Antonio. “The view that pathogens might be one of several paths leading to Alzheimer’s disease fits my current thoughts of amyloid and tau being critical brain responses to injury, instead of the initiators.”
That, he says, is why years of efforts to treat Alzheimer’s by removing those proteins have seen few results: they are symptoms of the disease, not its cause. “This is a further turning point in the understanding that infections and inflammation can be at the heart of Alzheimer’s disease.”
Nana Oforiatta-Ayim’s “Cultural Encyclopedia Project” will chronicle historical and contemporary art, music and literature from each African country.
Ghanaian writer and art historian, Nana Oforiatta-Ayim, was a PhD student back in 2009, when she first conceived the idea of creating a comprehensive archive of African art and culture.
“I would go to the underground library vaults, and I would find theses that were so brilliant and interesting, and yet no one was looking at it and it is so valuable, she tells The New York Times. “I would get completely sidetracked reading about things like the technology of kente cloth. And at the same time I was also thinking that the narrative that is told about Africa is still the backward narrative: no innovation, it’s ahistorical and stuck. Yet with everything I was reading, it was stories of innovation, of knowledge, of technology.”
Now, Oforiatta-Ayim’s idea is coming to life through her “Cultural Encyclopedia Project,” which will chronicle art from each African country, hence its 54 separate volumes. The first volume will be an internet-based repository of historical and contemporary Ghanaian art, literature music and more, reports The New York Times.
The project, which received a $40,000 grant from the Los Angeles County Museum in 2015, aims to help preserve the creations of African artists and help build knowledge about the Continent’s history.
It’s an immense undertaking, and each countries entry will likely take a couple of years to complete, but Oforiatta-Ayim has already created a plan on how to roll out future volumes. “So if other countries are going to take it on, then we are going to have a manual like, ‘this is how we collect things, this is what we did wrong and this is what we did right.’ There is no reason that, once we have the manual, there can’t be five countries at the same time working. So what I am doing is building teams in different countries,” she says.
There will also be art exhibits to accompany the online encyclopedia, the first of which premiered last week at Oforiatta-Ayim’s ANO gallery and research institution, in conjunction with Ghana’s 60th independence day.
The significance of the groundbreaking project is certainly not lost on those involved in its production. “What makes up the culture itself? And that is why it is open-ended and it is widespread in music, arts, language, dance. Every possible aspect is used and usable. It’s trying to tell your own stories and taking hold of your narrative,” said Nigerian musicianKezia Jones, who’s one of the encyclopedia’s contributors.
The “Cultural Encyclopedia Project” is about reclaiming African history, but it’s also about expanding knowledge of history and culture within the continent as well. It is such an important thing,” says David Adjaye.”Because actually East Africans don’t know about West Africans’ culture, and West Africans don’t know about North Africans’ culture, and North Africans don’t know about Southern Africans’ culture — and I am being simplistic here — but it is very hard. So this writing and forming of identity of the continent is really important.”
The health benefits of breast milk have long been flouted, but experts are now testing whether a compound found in mother’s milk could help treat cancer.
The accidental discovery of the effects of a compound found in breast milk, and nicknamed Hamlet, could mean a more effective and targeted way to kill cancerous tumour cells.
Researchers from the University of Lunt in Sweden have revealed some positive results from studying the effects Hamlet has on bladder cancer patients.
In the early trials, those injected with the compound began to shed dead tumour cells through their urine within days.
“There’s something magical about Hamlet’s ability to target tumour cells and kill them,” Professor Catharina Svanborg told Mail on Sunday.
But the discovery came completely by accident while the team was researching antibiotics.
“We were looking for novel antimicrobial agents, and new breast milk is a very good source of these,” professor Svanborg continued. “During one experiment we needed human cells and bacteria to be present, and we chose human tumour cells for practical reasons.”
“To our amazement, when we added this compound of milk, the tumour cells died. It was a totally serendipitous discovery.”
Researchers believe that a reaction takes place with breast milk when it hits the gut. It produces a protein called alpha-lactalbumin, which targets cancer cells.
The breast milk compound targets cancer cells alone, offering an alternative to chemotherapy and radiotherapy treatments, which can damage both healthy and cancerous cells in the body.
The scientists hope the breast milk compound could also help bowel and cervical cancer patients. A trial of the Hamlet substance against a placebo is currently being planned to test the promising benefits of the compound.
Applied Channel Theory in Chinese Medicine demonstrates how a deeper understanding of the interrelationship between organ and channel theory can lead to more precise diagnoses and better clinical results. This book is a collaboration between Wang Ju-Yi, one of modern China s most respected scholars, teachers, and practitioners of traditional Chinese medicine, and his American apprentice and practitioner, Jason Robertson. While most textbooks focus either on the functions of the organs in basic physiology or on the uses of the channels in treatment, this book shows the essential relationships between the two. Theory and practice are connected through a detailed discussion of a channel palpation methodology developed by Dr. Wang, which leads to more precise and effective point selection, location, and technique. Applied Channel Theory in Chinese Medicine was developed during Mr. Robertson s apprenticeship with Dr. Wang in Beijing, and is presented in a unique and highly readable format that preserves the intimacy of dialogue between apprentice and teacher, with questions and answers, narratives, and case studies.