German Company Developed Plant-based Alternative to Blue Fin Tuna

Anna Starostinetskaya wrote . . . . . . . . .

Germany-based food technology startup Kuleana recently developed Akami, a plant-based alternative to blue fin tuna. Kuleana is working on next-level fish alternatives in order to solve many problems in the traditional seafood industry, including overfishing, plastic pollution, fish fraud, human slavery, and human health concerns.

“Consumers have growing health concerns associated with consuming apex predators such as tuna because of their concentrations of mercury, micro plastics, and dioxins,” Kuleana CEO Jacek Prus said. “When it comes to consuming raw fish, bacteria and parasites are also on people’s minds.”

A recent study carried out by researchers at the University of Washington found that many species of fish now carry 283 times more parasitic worms than in the 1980s.

While Prus is not disclosing many details of the company’s proprietary process until appropriate patents are in place, he revealed that the nutritional profile of Akami closely resembles its animal counterpart. It is made with a combination of algae, sea water, koji, and vegetable proteins that undergo “traditional processing technologies in unconventional ways.”

Kuleana’s plant-based fish will be priced competitively to animal-based tuna and sold frozen in the foodservice sector to further minimize food waste by extending its shelf life.

he company is currently speaking with distributors in Europe, Asia, the United States, and Brazil in hopes of getting its plant-based fish to sushi and poke restaurants.

“Because we’ve focused on developing such a high-fidelity product, we’re convinced that it will help to get tuna off the table,” Prus said. “We’ve found that in order to truly replace a product, the substitute has to be at least as good in the fundamentals of taste, cost, and convenience.”

Source: Veg News

Butternut Squash with Pickled Red Onion and Herbed Salsa


2 lbs butternut squash
1 tsp extra-virgin olive oil
1/3 cup crumbled plain goat cheese

Pickled Red Onion

1/2 cup rice vinegar
1 tsp finely grated lime zest
1 tsp maple syrup or honey
1/2 tsp crushed red pepper flakes
1/2 tsp kosher salt
1/2 red onion, halved and very thinly sliced

Herbed Salsa

1/2 cup packed fresh Italian parsley
1/4 cup packed fresh mint leaves
1/4 cup packed fresh cilantro leaves
1/4 cup extra-virgin olive oil, plus extra
1 large garlic clove, smashed and minced
1 Tbsp fresh squeezed lime juice
generous pinch of crushed red pepper flakes


  1. Preheat oven to 425ºF (220ºC). Line baking sheet with parchment. Set aside.
  2. Peel butternut squash to bright orange flesh. Thinly shave top and bottom from squash and cut horizontally down middle to form 2 halves. Scoop out seeds and discard. Brush cut sides of squash with oil and place cut side down on prepared baking sheet. Bake in oven for 15 to 20 minutes, or until you can almost pierce it with a paring knife.
  3. While squash bakes, in small saucepan, heat rice vinegar. Pour into 1 cup heatproof glass jar, such as a canning jar, and stir in lime zest, syrup, 1/2 tsp crushed red pepper flakes, and salt.
  4. Stir to dissolve salt. Stir in onion and press down to immerse slices in vinegar. Cover and set aside. Onion can be refrigerated for a couple of weeks.
  5. After squash has been roasting for 15 minutes, remove from oven. On cutting board, place halves cut side down. Using very sharp knife, carefully cut 1/4 in (6 mm) wide slices crosswise into squash, being careful not to cut all the way through. Slide long spatula under sliced squash and return halves to baking sheet.
  6. Return to oven and continue to bake for 20 more minutes or until slices are completely tender but not falling apart.
  7. To prepare Herbed Salsa, in mini blender, combine herbs, oil, garlic, lime juice, and crushed red pepper flakes. Pulse until finely ground. Add a splash of water for thinner mixture. Add pinch of salt, to taste, if you wish. Store in tightly covered container for up to 1 week. Makes about 1 cup.
  8. To serve, remove squash from oven and place onto heated serving platter. Spoon some pickled onions and salsa overtop. Top with crumbled goat cheese and splash with a little extra olive oil, if you wish.

Makes 6 servings.

Source: Alive magazine

In Pictures: Home-cooked One-pot Vegan Meals

Foods That May Protect Against Dementia

Sari Harrar wrote . . . . . . . . .

Older adults who munched, crunched, and sipped the most flavonols—beneficial compounds in fruit, vegetables, tea, and wine—were 48 percent less likely to develop Alzheimer’s disease than people who consumed the least, according to a January 2019 report in Neurology. “This observational study does not prove cause and effect, but it adds to the idea that food is very important for brain health,” says the study’s lead author, Thomas M. Holland, MD, a researcher at Rush University in Chicago.

Dr. Holland and colleagues tracked 921 women and men for three to nine years, using yearly cognitive and memory tests plus in-person medical exams to diagnose dementia likely caused by Alzheimer’s. Participants—who had no signs of dementia at the start of the study—filled out annual food questionnaires, which the scientists used to estimate daily flavonol intake. Those who consumed at least 15.3 milligrams of flavonols—the amount in a small leafy green salad, one serving of cooked vegetables, or a half-cup of berries—per day had the lowest risk even after researchers adjusted for exercise levels, education, mentally stimulating activities, and the APOE4 gene, which increases the risk of developing Alzheimer’s in late life.

“Flavonols have anti-inflammatory and antioxidant properties,” Dr. Holland explains. “Antioxidants help destroy free radicals, which damage cells. Anti-inflammatories reduce inflammation, a natural process that can damage cells if it is overactive or sustained for too long.” In animal studies, flavonols boosted memory and learning and decreased Alzheimer-like brain changes.

“The study strengthens the argument for a potentially beneficial role of fruits and vegetables in brain function and provides an additional reason to consume them,” says Nikolaos Scarmeas, MD, associate professor of clinical neurology at Columbia University in New York City and the National and Kapodistrian University of Athens, Greece, who was not involved with Dr. Holland’s study.

“Flavonols may hold promise for promoting brain health,” says David Seres, MD, associate professor of medicine at the Institute of Human Nutrition at Columbia University in New York City. “But we need long-term, randomized, controlled studies involving thousands of people willing to follow a diet for several years to show that flavonols affect the human brain and that those benefits reduce the risk for Alzheimer’s.”

One such study is the US Pointer trial, which began earlier this year. During the two-year intervention, which involves 2,000 participants, researchers will investigate the effects of a healthy diet, exercise, brain-stimulating activities, socialization, and controlling cardiovascular conditions (such as high blood pressure) on Alzheimer’s disease and dementia risk. It’s based on the Finnish Geriatric Intervention Study to Prevent Cognitive Impairment and Disability, known as FINGER, in which participants who changed their habits experienced significant improvement in their thinking and memory compared with a control group.

“We estimate results in six or seven years,” says Dr. Holland, assistant trial director and medical advisor for the study’s branch at Rush University.

Until then, experts agree that a healthy diet is important for preventing poor blood circulation in the brain, which increases the risk of stroke, subtly damages small blood vessels, and contributes to vascular dementia, the most common cause of dementia after Alzheimer’s disease. (Often people have both vascular dementia and Alzheimer’s.)

To keep your brain in good shape, the experts recommend these lifestyle shifts:

Adopt healthy habits. “Flavonols are just one component of a healthy diet, and a healthy diet is just one part of prevention,” says Dr. Holland. An easy checklist to follow to lower the risk for cerebrovascular disease is the American Heart Association’s “Simple 7”: Eat healthy, exercise, quit smoking, maintain a healthy weight, prevent or treat high blood pressure, check for and treat high blood sugar, and avoid or treat high cholesterol. Also, remain socially engaged and participate in brain-stimulating activities. In a Mayo Clinic study published in Neurology in August 2019, older adults who played card games, did crossword puzzles, used a computer, or did crafts had a lower risk for developing mild cognitive impairment than those who didn’t.

Modify your meals. A good diet includes more produce and whole grains and less added sugar and saturated fats. “Try having a salad containing raw leafy greens every day or every other day, plus another cooked vegetable you like and some berries every day,” suggests Dr. Holland. “Choose colorful fruits and vegetables, so you get a wide range of vitamins, minerals, and other beneficial bioactives—components such as flavonols that influence physiological and cellular activity in the body.” Cook with seasonings like fresh dill, oregano, parsley, and tarragon; they all have flavonols. Tea, olive oil, oranges, and red wine contain small amounts of flavonols, but they were among the foods that contributed most to participants’ total intake in the study.

Forgo supplements. “Although supplements may be needed for certain medical conditions, they are not a stand-in for healthy foods, which also provide vitamins, minerals, fiber, and healthy fats,” says Dr. Holland.

Flavonol-Rich Foods

In their flavonol study, researchers at Rush University in Chicago found that people who consumed the most flavonols overall had a lower risk for an Alzheimer’s disease diagnosis than those who consumed the least. You won’t find flavonols listed on the nutrition panel of food packages, but according to the US Department of Agriculture, these foods contain them:

  • Almonds
  • Apples, dried
  • Apricots, dried
  • Arugula
  • Asparagus
  • Beet greens
  • Black beans
  • Blueberries
  • Broccoli
  • Brussels sprouts
  • Chinese cabbage
  • Collard greens
  • Cowpeas
  • Cranberries
  • Endive
  • Figs, dried
  • Golden raisins
  • Kale
  • Kidney beans
  • Kohlrabi
  • Mustard greens
  • Okra
  • Onions
  • Pears, dried
  • Pink beans
  • Pinto beans
  • Radicchio
  • Red cabbage
  • Rutabaga
  • Salsa
  • Scallions
  • Sour cherries
  • Spinach
  • Sun-dried tomatoes
  • Swiss chard
  • Tomato paste
  • Watercress
  • White beans
  • Zante currants

Source: Brain&Life

Gene Variant Staves Off Alzheimer’s in Some People

Bruce Goldman wrote . . . . . . . . .

People with a gene variant that puts them at high risk for Alzheimer’s disease are protected from its debilitating effects if they also carry a variant of a completely different gene, Stanford University School of Medicine investigators report in a large new study.

Their findings, to be published Apr. 13 in JAMA Neurology, suggest that a substantial fraction of the estimated 15% of Americans carrying the high-risk gene variant are protected to some degree from Alzheimer’s disease by a variant of the other gene. (A gene will often come in a variety of versions, or variants, that can produce different traits.)

The findings also may help drug developers better identify clinical trial participants and treatments for what, despite billions of dollars spent in pursuit of effective therapies, remains a disease without a cure.

About 5 million Americans — including roughly 1 in 10 people age 65 or older and one-third of those age 85 or older — have symptomatic Alzheimer’s disease. Even larger numbers have a subtler precursor called mild cognitive impairment. About half with this condition move on to full-blown Alzheimer’s. There are medications that can slow development of cognitive symptoms somewhat, but no available drugs prevent the disease’s progression or extend patients’ lives.

What causes Alzheimer’s isn’t well understood. There are probably numerous factors. But scientists have known for three decades about one main contributor to the disorder: a gene variant, ApoE4, that’s more than three times as frequent in Alzheimer’s patients than among people without the disease.

“While 15% of healthy people have the ApoE4 gene variant, it’s present in more than 50% of Alzheimer’s patients,” said Michael Greicius, MD, MPH, associate professor of neurology and director of the Stanford Center for Memory Disorders. “One copy of ApoE4 triples or quadruples your risk, compared with no copies. If you’re carrying two copies, your risk goes up tenfold.”

Greicius is the senior author of the study. Postdoctoral scholar Michael Belloy, PhD, is the lead author.

Not all ApoE4 carriers develop Alzheimer’s disease

“Having one or two copies of ApoE moves the age at which you get sick earlier by five to ten years,” Greicius said. “But, it turns out, not all ApoE4 carriers are destined to develop the disease. The gene variant we studied protects you from getting Alzheimer’s.”

A hallmark of Alzheimer’s is the aggregation in the brain of gummy deposits, or plaques, composed of a protein called beta-amyloid. Amyloid aggregation starts more than 10 years before symptoms appear.

“By the time someone is symptomatic, the amyloid horse is out of the barn,” Greicius said.

Recent technological advances have enabled the early prediction of Alzheimer’s onset by analyzing beta-amyloid levels and other protein levels in cerebrospinal fluid, and by detecting the buildup of Alzheimer’s plaques in the brain via imaging. These biomarkers make it possible to predict the disorder’s onset before outward symptoms become apparent, or to confirm diagnoses already reached on the basis of behavioral observations.

Yet even having two copies of ApoE4 by no means ensures that a person will develop Alzheimer’s. Some such people live to age 85 or 90 without symptoms; they’re protected, somehow, from the debilitating effects of this gene variant.

Greicius wondered why. Did some of these people share genetic variants that protect them?

The role of klotho

He and his collaborators focused on a variant of a gene for a protein called klotho. High blood levels of klotho predict longevity in animal studies. There’s also evidence for this in humans. For complicated reasons, carrying a single copy of the klotho variant — a genetic status referred to as heterozygous — but not two copies increases circulating levels of the klotho protein.

To assess the relationship between klotho-variant status and ApoE4-asociated Alzheimer’s risk, the researchers combed through publicly available databases for data on 22,748 ApoE4 carriers with and without symptoms of Alzheimer’s disease. All subjects were age 60 or older and of Northwestern European ancestry.

The researchers tallied the likelihood of those subjects with or without a single copy of the klotho variant winding up with Alzheimer’s symptoms versus remaining asymptomatic. They tracked asymptomatic ApoE4 carriers over time to determine whether those with a single copy of klotho were less likely to have developed Alzheimer’s symptoms. They also analyzed about 650 subjects to see if those with a single copy were less likely to develop cerebrospinal beta-amyloid levels or beta-amyloid brain deposits predicting the disease’s onset.

The results were unambiguous.

“In this ApoE4 carrier group, carrying one copy — but not two — of the klotho variant reduced Alzheimer’s risk by 30%,” Belloy, the study’s lead author, said. It substantially slowed the progression from symptom-free status to signs of mild cognitive impairment or outright Alzheimer’s disease. And it lowered the beta-amyloid burden in the brains of ApoE4 carriers who had not yet progressed to dementia.

Some 25% of Americans are heterozygous for the protective klotho variant. (A much smaller share have two copies, and the rest have none.) Genetic testing for klotho status among ApoE4 carriers could provide a better predictor of Alzheimer’s risk in people with the ApoE4 variant, Greicius said.

In addition, drug companies will want to consider excluding patients with a single klotho copy in their clinical trials to maximize the contrast in outcomes among ApoE4-positive participants receiving or not receiving an experimental treatment, Greicius said.

These trials often preferentially recruit ApoE4 carriers, who are predisposed to Alzheimer’s, in order to make it easier to detect within a reasonable time frame whether an experimental drug works. By eliminating prospective participants who carry ApoE4 but are potentially protected from Alzheimer’s by the klotho variant pinpointed in the new study, researchers can hope to get a clearer picture of a test drug’s value.

Learning more about how the protective gene variant works may also lead to a more sophisticated understanding of ApoE4’s debilitating effect on cognition — and, importantly, help researchers to zero in on therapeutic targets for the prevention or mitigation of those effects, Greicius said.

Source: Stanford Medicine

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