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Scallions Are Easy to Grow in Your Kitchen or Garden

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Scallions are a member of the Allium family, joining garlic, leeks, shallots and onions. They’re often used to add a bit of color or a garnish to a dish but are often overlooked for their nutritional value and overshadowed by other ingredients. Like others in the family, scallions contain sulfuric compounds designed to protect them from predators.1

The word scallion is derived from the Greek askolonion,2 referring to an ancient Palestinian port considered the home of the onion. However, it is now known onions are native to Asia. The word shallot is also derived from the word askolonion, meaning scallion in Australia, Canada and the U.K. Shallots are a completely different species in the U.S.

Although believed to originate in Asia, seeds of the onion plant have been discovered in Egyptian tombs dating 3200 B.C.3 According to the National Onion Association,4 King Ramses IV was entombed with onion bulbs in his eye sockets, possibly because some ancients believed onion scent carried magical powers to prompt the dead to breathe again.

Scallions are a member of the onion family, but may easily be confused with chives, green onions, spring onions and shallots. Before planting indoors or in your garden, let’s identify the scallion.

How to Identify a Scallion

The scallion is a young onion, sometimes called green onions. It has a white base and a long green stalk resembling chives. The plant will have stringy white roots, long tender green leaves and a stiff white stalk with no bulb. The plants are grown in bunches and harvested young.

A scallion has a mild onion flavor — not as intense as regular onions — and may be used raw or cooked. Spring onions look like scallions, but they have a small bulb base.5 They are a more mature version and may be planted as seedlings in the late fall and harvested in the spring, hence their name. Spring onions often taste sweeter than regular onions, but the greens are more intense than scallions.

Although they may look similar, chives6 are a different species. They are often used as a garnish in omelets, soups and salads. Botanically, they are classified as an aromatic grass. A true shallot is a bulb with a more delicate garlic flavor than onion flavor. It’s believed to have originated in Asia Minor7 and although they’re both from the onion family, they’re different varieties.

In many cases, you may substitute one for the other in a recipe, but you’ll experience a different flavor.8 Shallots have a thin outer layer of skin making it appear more like an onion than a scallion does. They grow in a similar manner to garlic — in clusters with a head or a bulb containing multiple cloves.

Growing Scallions in the Garden

Scallions may be grown indoors or outside. Most perennial scallions thrive in hardiness zones9 3 to 9 and enjoy full sun. They may handle partial shade but also require regular watering so it’s important not to plant them in hot dry soil.10

When starting from seed, consider planting indoors five or six weeks before the last frost or waiting until the soil begins warming before sowing directly in your garden. Plant the seeds thickly 1 to 1 1/2 inches deep, whether in the garden or in a flat indoors.11

Like other types of onions, scallions’ seeds may germinate slowly and poorly. The plants require constant moisture in well-draining soil, so they aren’t sitting in a puddle of water. When starting indoors, harden them off as the roots begin to fill the cell pack.

Hardening gives the seedlings time to become accustomed to the outdoors. Start on a mild day with two to three hours of sun exposure, adding a few hours every day. If the temperature drops below 40 degrees Fahrenheit (F), bring them indoors.12 Scallions have a shallow root system so it’s important to keep them watered after planting in the garden.13

You may enjoy a continual harvest by succession planting every three to four weeks. Adding a side dressing of organic fertilizer helps to keep them green and growing throughout the summer. Your crop will also appreciate being kept weed-free. If you’re growing perennial scallions, apply a layer of mulch in the fall and remove it in the spring for an earlier crop.14

Regrow Scallions Inside for All-Year Flavor

Once harvested, you may reroot your scallions indoors, or even use the ones you’ve purchased from the grocery store. Leave a couple of inches of the stem attached to the roots and add them to a couple of inches of water in a glass. Make sure the roots are pointed down and the stems are pointed up. Change the water every two to three days.15

Within seven to 10 days you’ll have another set of green tops. But the plant is not done yet! Keep the scallions in a glass of water near a source of sunlight and you’ll enjoy a couple more harvests from the same plant.

Scallions May Be Either Perennial or Biennial

Scallions may be either perennial or biennial.16 Annual plants complete their entire life cycle in a single season. Perennial plants go from seed to seed within one season but do not die at the end of the season.

Sometimes a plant classified as a perennial may be grown as an annual in colder climates when the winter kills them off. However, by definition, a perennial plant may be expected to live at least three years and, in some cases, longer,17 although not all perennials are able to withstand winter temperatures.

Between the category of annual and perennial is a biennial. These plants are shorter-lived than perennials, taking two growing seasons to complete their life cycle.

In the classic sense, the biennial produces only foliage in the first growing season. It is not until the second year it produces a flower and seeds. Parsley, some onions, beets, broccoli and cabbage are common biennial vegetables.18

Pick, Store and Slice Your Scallions for the Best Flavor

You’ll find scallions in the grocery store produce section throughout the year, but they are at their peak during the summer and spring.19 Their flavor will be mild when they’re young, so you may start harvesting as soon as the plants reach 6 inches in height and have the width of a pencil.

Harvest the whole plant by pulling it out, roots and all.20 If you have planted a perennial variety, consider thinning only and harvesting in the second year. In the second year, consider dividing the roots and replanting one or more of the divisions for a larger harvest the following year.21

Once you’ve brought the plants inside, store them in the refrigerator, in a jar with about an inch of water. Place a bag over the greens and secure it with a rubber band. This helps to keep the greens from wilting and maintain a fresh flavor.22

Change the water every day or two so it doesn’t get stale. In the refrigerator, scallions may last a little more than a week. If you plan to use them in stews and soups, they may be sliced and frozen. This changes their texture when they’re thawed, which makes them best used in cooked dishes after freezing.

You’ll retain better flavor when the scallions are sliced and not chopped. According to Master Class,23 the best process for slicing scallions is to use the entire length of a sharp blade. Start by laying scallions in a single layer on your chopping board.

Place the tip of the blade against the cutting surface and then steadily pulled the blade across the scallions. Downward pressure on the leaves bruises them, affecting the flavor.

Scallions Add Flavor and Nutrition

The age and type of the scallion you use will determine the flavor. These vegetables not only add something unique to your dishes, they also provide a variety of health boosting vitamins and minerals to help protect your health, including:24

Vitamin A — This antioxidant helps fight inflammation and damage caused by free radicals. It helps maintain your immune system function, slows the aging process, promotes healthy vision and skin, and improves bone health. Deficiency may lead to night blindness, higher risk of infection and infertility.25

Vitamin C — This water-soluble vitamin acts as a powerful antioxidant, helping to improve heart health, boost immune system function, regulate blood sugar levels and fight viral illnesses. It may also help reduce the risk of the common cold, cancer, osteoarthritis and age-related macular degeneration.26,27

Vitamin K — This helps lower the risk for cardiovascular calcification, heart disease and stroke, and plays an important role in blood clotting.28

Folate — This B vitamin plays an important role in the function of DNA and other genetic materials and may help reduce the risk of neural tube defects in babies, as well as preterm birth, cancer, heart disease and stroke.29

Potassium — This mineral balances electrical and chemical processes in your body, which in turn helps maintain proper muscle contractions, transmit nerve impulses, regulate blood sugar levels and improve blood pressure.30

Iron — Iron plays a role in the formation of hemoglobin, cell growth and differentiation, metabolism, endocrine and brain function, energy production, and immune health.31

Tasty Ways to Use Scallions

Scallions are versatile ingredient you may use when you want to lend a bit of onion flavor without the pungency of regular red or yellow onions. They can be sprinkled over soup, tossed into salads or added to sandwiches.

If you don’t have scallions at home or those in your garden are not yet ready for harvesting, there are several other members of the allium family you may use as a substitute, including:

  • Leeks — These vegetables taste stronger and have a tougher texture than scallions so it’s best to use them in cooked dishes.
  • Shallots — Ideal for cooked dishes, the flavor may be pungent when used raw.
  • Chives — These are often mistaken for scallions and may be used as a substitute. They have a mild flavor as do scallions, but sometimes do better in raw dishes than in cooked.
  • Ramps — Also called wild leeks, ramps have a strong onion and garlic flavor combination best for cooked dishes.

Scallion pancakes are a classic Chinese dish that is chewy, crunchy and savory, all at the same time. It may be eaten alone or with a dipping sauce of your choosing. This recipe was adapted from All Recipes.32

Scallion Pancakes

Prep Time: 20 minutes Cook Time: 20 minutes Total Time: 1 hour 10 minutes

Ingredients

  • 3 cups coconut flour
  • 1 1/4 cups boiling water
  • Coconut oil
  • Salt and pepper, to taste
  • 1 bunch scallions finely chopped

Procedure

  1. Create a dough mixture by mixing the coconut flour and boiling water in a large bowl. Knead the dough mixture until it forms a ball. Cover it and let it rest for 30 to 60 minutes.
  2. Evenly divide the dough into 16 pieces. Roll each piece into 1/4-inch-thick circles. Brush each circle with oil, season with salt and pepper and sprinkle with 1 teaspoon of chopped scallion.
  3. Take one of the dough circles, roll it up and then coil it into a round dough bundle. Pinch the open ends together to form a disc.
  4. Using the rolling pin or your hands, flatten the coiled dough bundles into pancakes that are around 1/4-inch thick.
  5. Heat 2 teaspoons of coconut oil in a large skillet. Fry the pancakes until golden brown, about two minutes on each side. Add more oil between batches, if necessary.

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Bone Marrow Transplant from Young to Old Mice Extends Remaining Life Span

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Here, researchers report on the results of transplanting cells from young bone marrow into old mice. The bone marrow came from genetically identical young mice, so there was no risk of rejection. Unlike the usual process for bone marrow transplants, there was no ablative chemotherapy to kill existing stem cells. This strategy led to a high degree of integration of young stem cells into the aged bone marrow, with cells of young origin making up a quarter of the bone marrow by the end of the study. This sizable integration is likely because old bone marrow has much smaller active stem cell populations, and thus their comparatively feeble efforts to produce daughter cells were outpaced by the activities of the transplanted cells.

As a result of this procedure, the maximum life span of the aged mice population was extended by nearly 30%. We can envisage many mechanisms by which this improvement can occur, such as greater production of immune cells, leading to a more active and competent immune system, or improved systemic signaling that may affect all organs, not just the bone marrow. The authors of the paper use these results to argue for the adoption of a similar therapy for old human patients, bone marrow transplantation without the ablative chemotherapy that characterizes its usual use in cancer patients, in order to achieve some degree of rejuvenation of tissue and immune system.


Increase in maximum lifespan (MLS) is the most significant indicator of hitting the basic mechanisms of aging, in particular, regarding age-related loss of stem cells and cell damage accumulation. In this study, a significant (30%) increase in maximum lifespan of mice was found after nonablative transplantation of 100 million nucleated bone marrow (BM) cells from young donors, initiated at the age that is equivalent to 75 years for humans. Moreover, rejuvenation was accompanied by a high degree of BM chimerism for the nonablative approach. Six months after the transplantation, 28% of recipients’ BM cells were of donor origin. The relatively high chimerism efficiency that we found is most likely due to the advanced age of our recipients having a depleted BM pool.

In addition to the higher incorporation rates, there are more reasons why the nonablative setting is preferable for old recipients. These are lesser risks of infections and of graft-vs-host disease, threatening to ablated patients, while graft rejection by nonablated recipients is less probable in the elderly than at a younger age because of naturally weaker immune system in the elderly. Even in the absence of histocompatibility, when allogeneic BM was used in a nonablative experiment instead of syngeneic BM, no lifespan shortening of the experimental group was observed.

Obviously, at an old age the immune system is already too passive to reject donor BM, but it still efficiently suppresses infection and graft-vs.-host reaction, which makes it unnecessary and undesirable to use ablative conditioning in the elderly. On the bases of the above and our data, we advocate a more rapid implementation of nonablative stem cell transplantation into the clinic not only for pathology treatment, but also for rejuvenation.

Link: https://doi.org/10.3389/fgene.2019.00310

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Ribosomal Biogenesis in Aging

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The ribosome is an important type of cell structure, the location of protein synthesis. Like most cell structures, ribosomes are recycled and rebuilt on a regular basis, and their construction takes place in the nucleolus. The paper here considers the evidence for altered rates or disruptions in the manufacture of ribosomes to relate to aging. There are clear associations, particularly for calorie restriction, which both slows aging and the pace at which new ribosomes are produced.


The nucleolus has gained prominent attention in molecular research over the past two decades, due to its emerging role in various cellular processes. Among them, the production of ribosomes is seemingly the most important, as it controls translation of all proteins in the cell and thus governs cell growth and proliferation. A number of studies have demonstrated that the disruption of virtually any step in ribosome biogenesis can result in cell cycle arrest, primarily through activation of the tumor suppressor protein p53. This particular process was recently termed as the Impaired Ribosome Biogenesis Checkpoint (IRBC).

Numerous studies presented a direct connection between dysregulated ribosome biogenesis and aging. For instance, the downregulation of ribosome biogenesis components or nutrient sensing pathways, which stimulate ribosome production, have been shown to increase the lifespan of multiple organisms including C. elegans, D. melanogaster, yeast, mice, and human. Therefore, enhanced ribosome biogenesis, visualized by enlarged nucleoli, is believed to accelerate aging. Indeed, consistent with this idea, the size of the nucleoli and the amount of rRNA increases during aging in human primary fibroblasts and a single, large nucleolus is often observed in senescent cells. Furthermore, fibroblasts isolated from patients suffering from the premature aging disease Hutchinson-Gilford progeria, have enlarged nucleoli and upregulated ribosome biogenesis.

Since the rate of protein translation is proportional to the rate of ribosome biogenesis it was suggested that upregulation of protein synthesis and disruption of global proteostasis is the mechanism through which ribosome biogenesis promotes aging. This theory is supported by studies showing that reduction in the rate of translation can increase lifespan, and furthermore that altered proteostasis is a hallmark of aging. Additionally, caloric restriction that has been shown to promote longevity, leads to the downregulation of ribosome biogenesis by several mechanisms.

Link: https://doi.org/10.18632/aging.101922

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Why is High Blood Pressure a Silent Killer?

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Why is High Blood Pressure a Silent Killer?
What’s the No. 1 risk factor for cardiovascular disease?

Is it high cholesterol? Stress? Being male? If you guessed high blood pressure (hypertension), you’re ahead of many of us. High blood pressure is one of the strongest risk factors for cardiovascular disease.1 However, a large number of people are unaware they have high blood pressure because they have no symptoms. No wonder they call it the silent killer.

Some risk factors for cardiovascular disease are not controllable. Older age, male gender, being postmenopausal and having a family history of the disease are uncontrollable risk factors. Fortunately for many, hypertension is among the controllable risk factors, in addition to smoking, being overweight, having diabetes or metabolic syndrome and the presence of elevated triglycerides and cholesterol.

How many of us know our average blood pressure reading and have had it recently measured? And how many who have been told they have high blood pressure have taken steps to control it?

Listen to Life Extension’s Michael A. Smith, MD, and Crystal Gossard, DCN, CNS®, LDN, as they review the importance of blood pressure in heart disease on www.LiveForeverish.com

What is normal blood pressure?

Normal blood pressure is less than 120/80 mm Hg. When the top number (systolic) is between 120 and 129 mm Hg and the bottom number (diastolic) is less than 80 mm Hg, blood pressure is elevated. Stage 1 hypertension occurs when the systolic reading is between 130 and 139 mm Hg and the diastolic reading is 80 to 89 mm Hg. Stage 2 hypertension is categorized as blood pressure greater than 140/90 mm Hg.2

Some evidence suggests that a target blood pressure of 115/75 mm Hg may be optimal.

Blood pressure meaning

Blood pressure is a measure of the pressure inside the blood vessels when the heart beats and when the heart is at rest.

Systolic blood pressure (the top number) measures the pressure inside the blood arteries when the heart beats. Diastolic blood pressure (the bottom number) reflects the pressure within the arteries when the heart is at rest between beats.

When pressure against the walls of the arteries is chronically elevated, it slowly damages the blood vessel lining. This makes the arterial lining susceptible to the buildup of plaque, which narrows the arteries and further increases pressure. If plaque ruptures, a blood clot can form that blocks narrowed arteries and impedes blood flow. When blockage occurs in the arteries that provide blood to the heart muscle, it is called a heart attack (myocardial infarction). When it occurs in the vessels that nourish the brain (due to blood-clot formation within the vessel, or a blood clot or plaque that traveled through the bloodstream), it is known as a stroke (cerebrovascular accident). High blood pressure can also cause a blood vessel in the brain to burst, which is known as a hemorrhagic stroke.3

Blood pressure measurement

Blood pressure is measured with a device known as a sphygmomanometer. Many of these devices are now electronic and can rapidly deliver accurate blood pressure measurements when applied to the arm or wrist. Because blood pressure changes throughout the day and may be higher than usual when measured in a medical practitioner’s office due to “white coat syndrome” (patient anxiety), monitoring blood pressure at home is an ideal way to gauge the effectiveness of one’s blood pressure maintenance program.

How to lower blood pressure

You’ve heard it before, but not smoking; maintaining a healthy weight; consuming a healthy diet (such as the DASH or Mediterranean diet) that contains a low amount of salt; engaging in regular, physician-approved exercise; and periodic monitoring of blood pressure by a medical professional, along with taking any prescribed medicines as directed, are essential for blood-pressure control.

Long-term stress management is also important. Learn how to handle life’s challenges in a positive manner. Meditation, walking or engaging in other relaxing activities can be helpful. Those who need more help may wish to ask their physicians about biofeedback therapy, which helps train the user to modify factors that affect blood pressure. In one study of biofeedback training among hypertensive patients, more than half lowered their blood pressure sufficiently enough to eliminate the need for medication.4 Similar reductions in blood pressure occurred among those who were not using blood pressure medications.

Foods to reduce blood pressure

As part of a comprehensive program to support healthy blood pressure, fruits and vegetables that are naturally low in sodium are good dietary choices. The Dietary Approaches to Stop Hypertension (DASH) diet recommends fruit and vegetables, whole grains and low-fat dairy products to lower blood pressure.5 Combining this eating pattern with sodium reduction has been associated with an even greater benefit.6

Nutritional supplements can be added to the diet to further improve blood pressure management. Research suggests that quercetin, stevioside (from stevia), fish oil, magnesium, pomegranate and potassium may be helpful.7-12

Although it often has no symptoms, high blood pressure is nothing to ignore. It’s critical to have blood pressure checked periodically, particularly as we get older. If you have high blood pressure, count yourself among the lucky individuals who have a health condition that is largely controllable. You’ll find that the recommended lifestyle changes that help control blood pressure will benefit many other aspects of health and well-being and lower the risk of other aging-associated conditions.

About Live Foreverish: Join Dr. Mike as he sits down with some of today’s leading medical, health and wellness experts to discuss a variety of health-related topics. From whole-body health to anti-aging and disease prevention, you’ll get the latest information and advice to help you live your life to the fullest. If you like what you hear, please take a moment to give Live Foreverish a 5-star rating on iTunes!

References

1. Kjeldsen SE et al. Pharmacol Res. 2018 Mar;129:95-99.
2. Whelton PK et al. Circulation. 2018 Oct 23;138(17):e426-e483.
3. Available at: https://www.heart.org/en/health-topics/high-blood-pressure/health-threats-from-high-blood-pressure
4. Fahrion S et al. Biofeedback Self Regul. 1986 Dec;11(4):257-77.
5. Chiu S et al. Am J Clin Nutr. 2016 Feb;103(2):341-7.
6. Sacks FM et al. N Engl J Med. 2001 Jan 4;344(1):3-10.
7. Larson AJ et al. Adv Nutr. 2012 Jan;3(1):39-46.
8. Liu JC et al. Pharmacology. 2003 Jan;67(1):14-20.
9. Geleijnse JM et al. J Hypertens. 2002 Aug;20(8):1493-9.
10. Rosanoff A et al. Magnes Res. 2013 Jul-Sep;26(3):93-9.
11. Asgary S et al. Phytother Res. 2014 Feb;28(2):193-9.
12. Filippini T et al. Int J Cardiol. 2017 Mar 1;230:127-135.

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An Interview with Jim Mellon of Juvenescence at Undoing Aging 2019

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The Life Extension Advocacy Foundation was not the only group conducting numerous interviews at the recent Undoing Aging conference in Berlin. Representatives of the German Party for Health Research were also set up with a camera and interviewer. The video here is their interview with billionaire Jim Mellon, one of the founders of Juvenescence. He is notable in our community for being one of the first high net worth individuals to fully and publicly back the SENS view of aging in both word and deed. SENS tells us that aging is caused by molecular damage, and that periodically repairing that damage is the way to produce rejuvenation.

Jim Mellon’s efforts go considerably beyond merely supporting rejuvenation research in the SENS Research Foundation network with philanthropic donations. His goal is to build an industry, attracting all of the necessary participants: entrepreneurs, venture funds, and more. To this end he published a book to popularize the opportunity that exists to treat aging as a medical condition, and raised a sizable fund in order to invest in the growth of the rejuvenation biotechnology industry. For the past year or more, Jim Mellon and the other principals Juvenescence have been investing aggressively in the first generation of startup biotechnology companies to work on ways to slow or reverse mechanisms of aging.

Jim Mellon at Undoing Aging 2019


Could you start by introducing yourself?

Ok, so my name is Jim Mellon, and I’m the chairman of a relatively new company called Juvenescence Ltd. I’ve been in the biotech business for about 12 years, and I’ve done other stuff in my career history, including fund management, mining, and German property investment. We still have our German property investment, some in Berlin some around the rest of Germany. The main focus at the moment is on our company, which is engaged in longevity science investment, which is called Juvenescence.

What is your motivation for that?

There are three motivations. One is self-preservation, so in other words a selfish interest in living longer, as I like living. The second is that this is obviously something that is going to have a huge human impact for the positive, so this is the ultimate ESG investment, if you know what ESG is. The third thing is that obviously we are a commercial organization and we are looking to make returns for our shareholders, of which we are the largest.

How would you describe your work and your engagement in aging research?

We have three partners in our business, and fifteen employees at the moment. The company started a year and a bit ago. We’ve raised about $160 million for our company, and we put in $35 million ourselves, of our own money. So it is quite well funded, and we’ve invested in 18 projects so far, ranging from small molecules, which is the specialization of our team, to stem cells, where as you may or may not know we own 46% of AgeX Therapeutics, which has been presenting here at this conference, and Aubrey de Grey is a senior vice president here, to organ regeneration. Our first product to go into a sick patient will be in the first quarter of next year, with a company called Lygenesis, which is working on liver regeneration.

So basically we are triaging investments with our team to find the most appropriate investments, to both advance science and get commercial products into the market, and we’re doing that as quickly as we can, given that this is a relatively early stage science from the commercial point of view. We expect our company to list on the New York Stock Exchange, on the NASDAQ, in early 2020. So we’re moving very, very quickly in this field.

What would you say to people in Germany who are indifferent to the whole aging research thing, and don’t know much about it?

Well that is a great question, who would not want to live, in a healthy condition, for longer, even if it is only five or ten years? That is now possible. So for the first time in human history it is possible to bioengineer humans to get that effect. All of the increases in life expectancy up to this point, as you know, have been due to environmental improvements. Now, for the first time, with the unveiling of the human genome, the identification of pathways, the use of animal models to manipulate those pathways, demonstrates that, for sure, something is going to work in prolonging human healthspan. We don’t know exactly what yet, but there are some human trials underway at the moment, so that gives us great optimism. We are very lucky to be the first cohort ever on the planet to have that indulgence, that we may be able to live longer and in a healthier condition.

We recognized that fairly early on. Most people, as you rightly point out, are indifferent to it, or don’t believe it. We certainly do believe it, and our history is a good one in biotech. We’ve set up a number of biotech companies. One is already listed on the New York Stock Exchange. It is about a $3 billion market capitalization. We set up that company four years ago, and it has a cure for migraine, which will be on the market in America next year. We can demonstrate that we can deliver new drugs and new therapies to human beings, and now we’re going to do that in the longevity space. So we’re very excited and very, very focused on that.

You need lots of money for that of course, and what the German Party for Health Research wants is much more money for research and development from the government. How much are we talking about? What would you recommend?

I don’t think there is any upper limit to the amount that could be usefully deployed. Obviously governments are cash constrained, so it is not just governments but individuals, corporations, and so forth that should get on to this bandwagon. We’re in the dial-up phase of the internet in the early 1980s. We’re in the very early stage of this industry. We’re at the front end of a huge investment curve. Money will start coming in: Samumed has raised a great deal of funding, Calico has a great deal of funding from Google and Abbvie. We’ve raised quite a large amount of funding, and there are other companies such as Unity Biotechnology and resTORbio that have raised funds.

But this is just the beginning of what will be an enormous amount of funding coming in. The UK government – I’m a British citizen – has devoted GBP300 million to this area under the auspices of Oxford University and John Bell. The German government should do the same. Governments across Europe should do the same, so that this is not just an Americn science, not just something that belongs to California or to Texas. It needs to be a universal science. So I fully endorse the aims and motivations of your party and I wish you very well in the forthcoming elections.

Let’s go 20 years into the future: how do you want an 80 year old living in 20 years?

Well my father just turned 90 as an example, and he is in robust health. I want him to benefit from metformin and rapamycin and the coming therapies, and to maintain his healthy life span until at least 120. From a personal motivational point of view, I would like him to be as healthy as he is today, for a fairly advanced stage, in 20 or 30 years. I believe it to be possible. Just to show you how dedicated we are to maintaining him in good health, and others like him, we are having his 90th birthday party in Ibiza, which is not normally associated with raves for old people. Well, that’s where we are having the party!

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Antibiotics for 2 Months Increase Stroke and Heart Attack Risk

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Using antibiotics for an extended period of time during middle-age or later may increase the risk of cardiovascular disease in women.

The finding comes from a study published in the European Heart Journal, which revealed women aged 60 and over who used antibiotics for two months or longer had significantly increased risk of cardiovascular disease, including heart attack and stroke, compared to women who did not.1

According to a press release2 by the researchers, the results held true even after adjusting for other related factors, like obesity, other chronic diseases and diet and lifestyle. Antibiotic exposure leads to long-lasting alterations in gut microbiota, which may influence risk of cardiovascular disease.

Antibiotics Use Leads to Heart Risks

While the use of antibiotics in younger adults between the ages of 20 and 39 was not linked to heart risks, women aged 60 and older who used antibiotics for two months or longer were 32% more likely to develop cardiovascular disease than women who did not use such drugs.

Overall, among women in late adulthood who take antibiotics for two months or more, six per 1,000 would develop cardiovascular disease, compared to three per 1,000 for women who did not. Women in middle age (40 to 59 years) who used antibiotics for longer than two months also had a 28% increased risk of cardiovascular disease.

The women used antibiotics most often for respiratory infections, urinary tract infections and dental problems, although the results held true even after the reasons behind the usage were factored in. Lead study author Lu Qi, director of the Tulane University Obesity Research Center in New Orleans, stated in a news release:3

“By investigating the duration of antibiotic use in various stages of adulthood we have found an association between long-term use in middle age and later life and an increased risk of stroke and heart disease during the following eight years.

As these women grew older they were more likely to need more antibiotics, and sometimes for longer periods of time, which suggests a cumulative effect may be the reason for the stronger link in older age between antibiotic use and cardiovascular disease.”

Antibiotics’ role in wiping out beneficial gut bacteria was also highlighted as a likely reason for the increased heart risks. “Antibiotic use is the most critical factor in altering the balance of microorganisms in the gut. Previous studies have shown a link between alterations in the microbiotic environment of the gut and inflammation and narrowing of the blood vessels, stroke and heart disease,” Qi said.4

What Does Your Gut Health Have to Do With Your Heart?

It’s becoming increasingly common knowledge that antibiotics are an enemy to the health of your gut — so much so that even mainstream pharmacies may suggest you take probiotics, or good bacteria, along with a prescription for antibiotics in order to help protect your gut.

One of the risks of taking antibiotics is that it can allow unhealthy bacteria, viruses or other microorganisms to flourish in your gut, which can take a toll on your heart.

For starters, when the bacteria in your gut break down lecithin, a fat found in meat, eggs, dairy and other animal foods along with baked goods and dietary supplements, and its metabolite choline, it leads to the creation of a by-product called trimethylamine N-oxide or TMAO.5

TMAO encourages fatty plaque deposits to form within arteries (atherosclerosis), and the more TMAO you have in your blood the greater your risk of heart disease becomes. It’s not clear which types of gut bacteria lead to the formation of TMAO, but it’s suggested that probiotics may help to buffer the effect and thereby help prevent heart disease.

Another study published in the journal Atherosclerosis found that patients with inexplicably high amounts of arterial plaque, based on their age and risk factors for atherosclerosis, had higher levels of TMAO, p-cresyl sulfate, p-cresyl glucuronide and phenylacetylglutamine — metabolites produced by certain gut microbes.

On the other hand, people with unexpectedly low amounts of plaque, despite having traditional risk factors, had lower levels of these metabolic products. The differences could not be explained by renal function or poor diet.

Rather, there was a difference in gut microbiome between the groups. The researchers noted, “The intestinal microbiome appears to play an important role in atherosclerosis. These findings raise the possibility of novel approaches to treatment of atherosclerosis such as fecal transplantation and probiotics.”6

Some Antibiotics May Cause Fatal Heart Damage

One class of antibiotics known as fluoroquinolones may harm your heart by causing an increased risk of ruptures or tears in the aorta blood vessel. The aorta is the main artery in your body supplying oxygenated blood to your circulatory system.

In December 2018, the U.S. Food and Drug Administration (FDA) warned that fluoroquinolones taken by mouth or via injection could lead to these aortic dissections or ruptures of an aortic aneurysm that could lead to serious bleeding or death.7

The risk is so great that the FDA advised health care professionals to avoid prescribing such drugs, which include brand names Cipro and Levaquin, to people who have an aortic aneurysm or are at risk for an aortic aneurysm, including people with peripheral atherosclerotic vascular diseases, hypertension, certain genetic conditions such as Marfan syndrome and Ehlers-Danlos syndrome, and elderly patients.

Long-Term Antibiotics Use Linked to Colon Polyps

The gut alterations that occur as a result of antibiotics use may also influence your risk of cancer. In 2014, researchers linked antibiotics use to a slightly increased risk (8% to 11%) of developing colorectal cancer, also known as bowel cancer, possibly because of alterations to the gut microbiome.8

Likewise, past research has also shown that people with less bacterial diversity in their gastrointestinal tracts are more likely to develop colon cancer.9 Then, in 2017, research published in the journal Gut found women who had used antibiotics for two months or more were at an increased risk of developing colon polyps.10

Specifically, those who used the drugs for a total of at least two months in their 20s and 30s had a 36% increased risk of polyps compared to those who did not. Among women who used the drugs long-term in their 40s and 50s, the risk of polyps increased by 69%.11

Even taking antibiotics for 15 days or more, at any age range, was associated with an increased risk of polyps. Those researchers noted that antibiotics “fundamentally alter the gut microbiome by curbing the diversity and number of bacteria, and reducing the resistance to hostile bugs.”12

When Taking Antibiotics, ‘the Shorter the Better’

Antibiotics save lives when used appropriately, but the benefits must be carefully weighed against the risks, which can occur in both the short- and long-term. From 2010 to 2011, the U.S. Centers for Disease Control and Prevention (CDC) found that, of 262 million antibiotic prescriptions written by physicians, 30% were unnecessary.13

Antibiotics prescriptions for acute respiratory conditions were most often inappropriately prescribed, which is interesting since the featured study also found respiratory infections to be a common reason why older women took antibiotics for long periods. Viruses, against which antibiotics are useless, commonly trigger upper respiratory infections.

In the short term, 20% of adults prescribed antibiotics in the hospital experienced adverse side effects and 20% of those side effects occurred in patients who didn’t need the antibiotics in the first place.14 Further, every additional 10 days of antibiotic therapy led to a 3% increased risk of a related adverse event, so the longer antibiotics were taken, the higher the risk of adverse events became.

Further, just one course of antibiotics negatively alters your microbiome for up to a year,15 which is precisely why it’s crucial to only use antibiotics when absolutely necessary. In fact, previous research by Qi and colleagues found that one course of antibiotics leads to long-lasting adverse effects on gut health and increases the risk of antibiotic resistance.

Taking antibiotics for at least two months also increases the risk of death from all causes by 27% among women in late adulthood, compared to women who did not take the drugs.16 The women taking long-term antibiotics also had a 58% higher risk of death due to heart problems.

According to Qi, speaking of the featured study, “Our study suggests that antibiotics should be used only when they are absolutely needed. Considering the potentially cumulative adverse effects, the shorter time of antibiotic use the better.”17

Antibiotic-Resistant Disease Is on the Rise

Arguably, the greatest risk of antibiotics use is the spread of antibiotic-resistant disease. Every year at least 2 million Americans acquire drug-resistant infections and 23,000 die as a result. Many others die from conditions that were complicated by antibiotic-resistant infections.18

Worldwide, 700,000 people die every year due to antibiotic-resistant disease, and it’s estimated that more people will be affected by it than cancer by 2050.19 Already, tens of thousands of Americans may be vulnerable to life-threatening infections following surgery or chemotherapy due to antibiotic resistance.

One study estimated that up to 50.9% of pathogens that cause surgical site infections, and 26.8% of those that cause infections following chemotherapy, are already resistant to common antibiotics.20 If antibiotic effectiveness drops by even another 10%, it could result in 40,000 more infections and 2,100 additional deaths following surgery and chemotherapy each year.

A 30% drop in effectiveness could mean another 120,000 infections and 6,300 deaths annually, the researchers concluded.21 Worse still, if antibiotic effectiveness declines by 70%, the US could see 280,000 more infections and 15,000 more deaths as a result.

For the protection of your heart, your gut and your overall health, it’s important to carefully weigh whether every course of antibiotics you take is truly necessary. Meanwhile, agriculture remains a driving force behind the surge in antibiotic-resistant disease, both in regard to livestock living on concentrated animal feeding operations (CAFOs) as well as the spraying of antibiotics as pesticides on crops such as citrus.

To protect yourself, choose antibiotic-free, organic food and use antibiotics for medical purposes only when necessary. If you do have to take antibiotics, add more traditionally fermented and cultured foods to your diet to optimize your gut flora, and consider the use of spore-based probiotics, or sporebiotics, which are part of a group of derivatives of the microbe called Bacillus, have been shown to dramatically increase your immune tolerance.

I also recommend taking the beneficial yeast Saccharomyces boulardii after you’ve finished your antibiotics, to prevent secondary complications of antibiotic treatment, such as diarrhea.

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Clearance of Senescent Oligodendrocyte Cells as a Treatment for Alzheimer's Disease

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The accumulation of lingering senescent cells is one of the root causes of aging. These cells secrete signal molecules that rouse the immune system to a state of chronic inflammation, resulting in disarray of tissue function and the progression of age-related disease. Recent studies in mouse models of Alzheimer’s disease have shown that senescent microglia and astrocytes are important in the generation of neuroinflammation and tau pathology in this condition. The use of senolytics to remove these cells results in a significant reduction in pathology.

Here, researchers provide further evidence to show that accumulation of various types of senescent cells – and the inflammation that they generate – is likely a vital part of the bridge between early amyloid-β aggregation and later tau aggregation in Alzheimer’s disease. Decades of slow amyloid-β aggregation may act as the foundation of the far more serious later stages of the condition in large part because this process provokes greater levels of lingering cellular senescence than would otherwise occur.


The most common cause of age-related dementia, Alzheimer’s disease is marked by the aggregation of amyloid proteins, which can kill off surrounding neurons. The areas of amyloid accumulation and associated nerve cell death, called plaques, are a hallmark of the disease. Researchers found that a specific brain cell type, called oligodendrocyte progenitor cells, appears in high numbers near plaques. In a healthy brain, oligodendrocyte progenitor cells develop into cells that support nerve cells, wrapping them in a protective layer that heals injury and removes waste. The environment created by the amyloid proteins causes these progenitors to stop dividing and conducting their normal functions. In diseases such as Alzheimer’s, the oligodendrocytes instead send out inflammatory signals that contribute more damage to the surrounding brain tissue. “We believe the amyloid is damaging the neurons, and although the oligodendrocytes move in to repair them, for some reason the amyloid causes them to senesce rather than complete their job.”

The researchers suspected that if they could selectively remove malfunctioning senescent oligodendrocyte progenitor cells, they could slow Alzheimer’s disease progression. The researchers tested the concept in mice that were genetically engineered to have some of the characteristics of Alzheimer’s disease, such as aggregated amyloid plaques. To remove the senescent cells, the researchers devised a treatment with a mixture of two FDA-approved drugs: dasatinib and quercetin. Dasatinib was originally developed as an anti-cancer drug, and quercetin is a compound found in many fruits and vegetables. The drug combination was proven as an effective way to eliminate senescent cells in previous studies of other diseases. The researchers administered the drugs to groups of the Alzheimer’s mice for nine days, then examined sections of the mice’s brains for signs of damage and the presence of senescent oligodendrocyte progenitor cells.

They report that the mice treated with the drugs had approximately the same amount of amyloid plaques as mice that received no treatment. However, the researchers say they found that the number of senescent cells present around these plaques was reduced by more than 90 percent in mice treated with the drug combination. They also found that the drugs caused the senescent oligodendrocyte progenitor cells to die off. Together, these results show that the dasatinib and quercetin treatment effectively eliminated senescent oligodendrocyte progenitor cells.

The researchers next tested whether the physical benefits of the dasatinib and quercetin treatment could protect the mice against the cognitive decline associated with Alzheimer’s disease. To do that, the researchers fed the genetically engineered mice the dasatinib and quercetin drug combination once weekly for 11 weeks, beginning when the mice were 3 1/2 months old. The researchers periodically evaluated the mice’s cognitive function by observing how they navigated mazes. They found that after 11 weeks, control mice who got no drug treatment took twice as long to solve the maze as their counterparts treated with dasatinib and quercetin. After 11 weeks, the researchers again analyzed the brains of the mice and found 50 percent less inflammation in mice treated with dasatinib and quercetin, compared with nontreated mice. The researchers say these results show that eliminating senescent cells from the brains of affected mice protected cognitive function and reduced inflammation linked to Alzheimer’s disease-like plaques.

Link: https://www.hopkinsmedicine.org/news/newsroom/news-releases/restoring-brain-function-in-mice-with-symptoms-of-alzheimers-disease

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Amyloid-β Aggregation Accelerates Age-Related Activation of Microglia

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This open access paper is illustrative of present work on the role of microglial dysfunction and chronic inflammation in Alzheimer’s disease. The central nervous system immune cells called microglia become inappropriately inflammatory with age. A new consensus on Alzheimer’s disease is that initial amyloid-β accumulation causes far greater than usual chronic disarray and inflammatory signaling in the supporting cells of the brain, such as microglia, astrocytes, and oligodendrocytes. This in turn leads to the much more damaging tau aggregation and consequent damage and death of neurons.


Alzheimer’s disease (AD) is characterized by typical biochemical lesions (β-amyloid peptide [Aβ] plaques and tau tangles) accompanied by extensive cellular changes (neuronal dystrophic alterations, neuronal cell loss, astrogliosis, and microgliosis). Rare mutations in amyloid precursor protein (APP), presenilin 1 and presenilin 2 trigger Aβ plaque accumulation and are sufficient to induce the full biochemical and morphological signature of AD. While this clearly indicates a major role for Aβ in AD pathology even in these genetic forms, a decades-long asymptomatic phase is present. Thus, in addition to Aβ plaques, other pathological processes, either in response to or in parallel to Aβ accumulation, need activation to cause neurodegenerative disease.

The search for the genetic risk determinants in sporadic AD has highlighted the central role of non-neuronal genes in pathways that do not appear directly related to Aβ metabolism. Most of the genes associated with the ∼40 loci identified by genome-wide association (GWA) analysis or by rare variant sequencing studies are expressed in glial cells. Moreover, analysis of available single-cell transcriptome datasets for human brain cells reported an association between AD GWA signals and microglia as well as astrocytes. Analysis of regulatory networks of genes differentially expressed in AD patients indicates that immune- and microglia-specific gene modules are key contributors to AD pathology.

Thus, genetic and molecular evidence suggest that Aβ accumulation is the trigger of a series of pathogenic processes in which microglia play a central role. No consistent hypothesis, however, links the causality implied by the mutations in the amyloid pathway genes to the genetic risk linking sporadic AD to inflammatory pathways. One possible resolution is that amyloid pathology acts only as a trigger in sporadic AD; i.e., Aβ accumulation is necessary but insufficient to cause full-blown disease. The cellular response, determined by the genetic makeup of the patients, tilts the table from a rather benign Aβ proteopathy to the severe neurodegeneration with inflammation and tau pathology that characterizes AD. In this regard, further understanding of the microglia response to amyloid pathology and the role of risk factors for AD in this response is key.

Here, we set out to address in a systematic way the question of how microglia respond over time, in cortex and hippocampus, to progressive Aβ deposition and whether this is affected by the three major risk factors for AD, i.e., age, sex, and genetics. We use an App knockin mouse model, which displays progressive amyloidosis and microgliosis. We show that the microglial responses to Aβ pathology are complex but, surprisingly, largely reproducible cell states that are also appearing during normal aging, albeit slower and quantitatively more limited. Moreover, we show that microglia in female mice tend to react earlier and in a more pronounced way than microglia in male mice, particularly in older mice. Interestingly, the major response of microglia to amyloid pathology is enriched for AD risk genes, with Apoe expression, in particular, becoming highly upregulated. This is partially confirmed in human tissue.

Link: https://doi.org/10.1016/j.celrep.2019.03.099

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Repair Biotechnologies Raises a $2.15M Seed Round to Fight Age-Related Diseases

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As many of you know, Bill Cherman and I founded Repair Biotechnologies in 2018 with the intent of developing promising lines of rejuvenation research into clinical therapies. There are many opportunities given the present state of the science and far too few people working on them. This remains true even as large amounts of venture funding are entering the space; our field needs more entrepreneurs. I’m pleased to note that we’re making progress in our pipeline at Repair Biotechnologies, and have recently closed a seed round from notable investors in order to power us through to the next phase of our work.

What does the Repair Biotechnologies team work on? When we initially set out, after a survey of the field, we settled upon regeneration of the thymus via FOXN1 upregulation as the lowest of low-hanging fruit, a project with good evidence in the literature and the potential of a sizable upside to health in later life when realized. The thymus atrophies with age, and this is a major factor in the age-related decline of the immune system, as the thymus is where T cells mature. Reductions in the supply of new T cells eventually leads to an immune system packed with malfunctioning, senescent, and overspecialized cells that are incapable of defending effectively against pathogens and errant cells.

A little later we picked up development of a fascinating line of research relating to the vulnerability of macrophages to cholesterol. The pathologies of atherosclerosis are caused when macrophage cells become ineffective at clearing out cholesterol from blood vessel walls. They are overwhelmed by oxidized cholesterol in particular, but too much cholesterol in general will also do the trick. Macrophages become inflammatory or senescent, and die, adding their debris to a growing fatty plaque that will eventually rupture or block the blood vessel. By giving macrophages the ability to degrade cholesterol, we can in principle reverse atherosclerosis by making macrophages invulnerable to the cause of the condition. This is, we believe, a much better approach that that of trying to reduce cholesterol in the bloodstream.

Repair Biotechnologies Raises $2.15M Seed Round to Develop Drugs for Age-Related Diseases


Repair Biotechnologies, Inc. announced today $2.15 million in seed venture funding, to accelerate the preclinical development of its pipeline of drugs targeting thymus regeneration, cancer, and atherosclerosis. The $2.15 million in funding was led by Jim Mellon, the billionaire investor and chairman of Juvenescence Ltd. Also participating in the round are Emerging Longevity Ventures, Thynk Capital, and SENS Research Foundation.

“We are committed to developing treatments for the root causes of aging and its associated diseases through the damage repair approach,” said Reason, co-founder and CEO. “With this funding round, we will be able to further develop our therapies and validate them in animal models, bringing them closer to the clinic and patients.”

The thymus gland is vital to the adaptive immune system, but with age, the thymus shrinks, leading to a decreased immune cell production and a compromised immune system. Repair Biotechnologies is developing a therapy with the aim of reverting this atrophy of the thymus, which the company believes can be an effective treatment against some forms of cancer. Repair Biotechnologies’ second major project relates to atherosclerosis, which is caused by the accumulation of intracellular waste in arteries. While present therapies focus on reducing cholesterol, Repair Biotechnologies has licensed a technology to make the macrophage cells responsible for repairing arteries resilient to excess cholesterol, and thus able to repair atherosclerotic damage.

“SENS Research Foundation was founded to push forward proof-of-concept work demonstrating the validity of the SENS paradigm to the point at which people can actually do something with it. Now we’re seeing some of these technologies getting the recognition from investors that they deserve, which in turn is driving critical growth in the private-sector side of the field,” said Aubrey de Grey, co-founder and Chief Science Officer of SENS Research Foundation. “I’m thrilled to see Repair Biotechnologies taking things in this area to the next level.”

Nothing in this post should be construed as an offer to sell, or a solicitation of an offer to buy, any security or investment product. Certain information contained herein may contains statements, estimates and projections that are “forward-looking statements.” All statements other than statements of historical fact in this post are forward-looking statements and include statements and assumptions relating to: plans and objectives of Repair Biotechnologies’ management for future operations or economic performance; conclusions and projections about current and future economic and political trends and conditions; and projected financial results and results of operations. These statements can generally be identified by the use of forward-looking terminology including “may,” “believe,” “will,” “expect,” “anticipate,” “estimate,” “continue”, “rankings” or other similar words. Repair Biotechnologies does not make any representations or warranties (express or implied) about the accuracy of such forward-looking statements. Accordingly, you should not place reliance on any forward-looking statements.

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Why Children Are Getting Fatty Liver Disease

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Fatty liver disease is caused by excess fat in your liver. The medical term is hepatic steatosis. Your liver normally contains some fat, but when greater than 10% of the weight of the liver is fat, it’s called fatty liver. There are two main types: nonalcoholic fatty liver disease (NAFLD) and alcoholic fatty liver disease, also called alcoholic steatohepatitis.1

NAFLD may be suspected if a blood test shows higher levels of liver enzymes than expected. While the disease is found more frequently in adults, researchers are finding NAFLD is a growing concern in the pediatric community, which triggered at least one intervention study weaning participants off sugar to reduce obesity and Type 2 diabetes.2

Chief of gastroenterology, hepatology and nutrition at University of Southern California and Children’s Hospital of Los Angeles (CHLA), Dr. Rohit Kohli, commented,3 “Fatty liver disease is ripping through the Latino community like a silent tsunami and especially affecting children.”

While research demonstrates 25% in the U.S. have fatty liver disease,4 in the Latino community the rate is much higher. One study in Dallas, Texas5 examined 2,287 subjects from a multi-ethnic population and found 45% of Hispanics suffered from fatty liver disease. The ethnic differences in the frequency of disease in this study mirrors those in past studies for NAFLD-related cirrhosis.

Key Facts About Fatty Liver Disease

NAFLD is the type not related to heavy alcohol use and in this category there are two types: simple fatty liver, in which your liver has additional fat but little to no inflammation or damage, and nonalcoholic steatohepatitis (NASH), in which you suffer from inflammation and damage in the liver cells, as well as excess fat in your liver.

NASH may cause fibrosis or scarring of the liver and lead to cirrhosis or liver cancer. Researchers have not been able to point to a single cause of NAFLD, but they do know it occurs more commonly in those who have specific risk factors, including:6,7

Type 2 diabetes or prediabetes

Metabolic disorders, including metabolic syndrome

High levels of fats in the blood

Obesity

Middle-aged or older

High blood pressure

Rapid weight loss

Infections, such as hepatitis C

Exposure to some toxins

Gallbladder removal

Hispanic

NAFLD affects nearly 25% globally.8 However, as the rates of obesity and Type 2 diabetes rise, so do the rates of NAFLD. NAFLD is usually a silent disease, meaning most are unaware of the condition and have few or no symptoms. When symptoms are present, individuals may feel greater fatigue or have discomfort in the upper right-hand side of the abdomen.

It is important to distinguish between simple fatty liver disease and NASH since those with NASH experience damage to their liver cells, which increases the risk of progression to fibrosis, cirrhosis and liver cancer. According to Harvard Health Publishing,9 NASH cirrhosis is expected to top the reasons for liver transplants.

Sugar Passed in Breast Milk Predisposes Infants to Obesity

A new study10 is being led by Michael Goran, Ph.D., director of the diabetes and obesity program at Children’s Hospital Los Angeles. Last year, he discovered high fructose corn syrup (HFCS) sweetened beverages were passed through breast milk, potentially predisposing infants to fatty liver and obesity.11

Six weeks after giving birth, 41 participating women were randomized into two groups. One group consumed a readily available HFCS sweetened beverage and the other group consumed an artificially-sweetened control beverage. At each testing session, the mothers expressed milk every hour for six consecutive hours.

The researchers then measured the concentration of fructose, glucose and lactose in the breast milk. Changes were significant only for measurements of fructose, with comparisons showing HFCS beverages increased breast milk fructose at hour two, three, four and five hours after consumption. It is important to note breast milk normally does not contain fructose.12 Goran commented:13 

“Lactose is the main source of carbohydrate energy and breast milk is very beneficial, but it’s possible that you can lose some of that beneficial effect depending on maternal diet and how that may affect the composition of breast milk.

Other studies have shown that fructose and artificial sweeteners are particularly damaging during critical periods of growth and development in children. We are beginning to see that any amount of fructose in breast milk is risky.”

Dr. Robert Lustig, professor in the division of endocrinology at the University of California, is a pioneer in decoding sugar metabolism. He was among the first to bring attention to the fact that processed fructose is far worse for your metabolic system than other sugars. Fructose is broken down like alcohol in your body,14 triggering liver damage and causing mitochondrial and metabolic dysfunction.

This damage is very similar to that caused by ethanol and other toxins. Fructose also triggers severe metabolic dysfunction as it is readily metabolized into fat, far more so than other sugars. Researchers are finding exposure before birth may increase an infant’s risk of obesity leading to a higher risk of Type 2 diabetes and NAFLD.15

Gene Variant Increases Risk of Fatty Liver Disease

Before 2006, few knew children could develop NAFLD. Dr. Jeffrey Schwimmer, professor of pediatrics at the University of California San Diego, reviewed 742 autopsies of children and teenagers who had died from traumatic injury. He found an incidence of 13% with fatty liver disease, and 38% in those who were obese.16

The researchers concluded NAFLD was the most common liver abnormality in children aged 2 to 19. They suggested the identified risk factors should be considered in the development of protocols to screen children and adolescents who are at risk.

A study released in 200817 by a group of researchers from the University of Texas demonstrated a gene variant called PNPLA3 could increase the risk of fatty liver disease. Nearly 50% of Latinos have at least one copy of this high-risk gene, and 25% have two copies according to Goran.18

Goran then undertook another study, eventually demonstrating children as young as 8 who had two copies of PNPLA3 and who consumed high amounts of sugar had 2.36 times as much fat in their livers as children without the gene.19 In the clinical trial20 currently underway, his team first tests participating children for the gene and then uses an MRI to measure liver fat percentage.

The sugar consumption of the child is measured and cataloged and then a dietitian educates the family on the impact of sugar. The team does another MRI four months later to measure liver fat and assess the impact of the intervention.

Goran’s research and past studies21 have demonstrated early exposure to sugar and fructose likely contribute to obesity, diabetes and fatty liver disease as fructose enhances the body’s capacity to store fat.

Excess Fructose Triggers Obesity and Fatty Liver Disease

Results of a meta-review in Mayo Clinic Proceedings22 confirmed that not all calories are equal. The dogmatic belief that a calorie is a calorie has driven the weight loss industry and contributed to an ever-worsening history of health in the Western world.

Unfortunately, it continues to be a concept taught in schools, even though we now know it’s false. The source of the calories does indeed have a significant impact on your health and weight. In the review, the researchers evaluated how different calories affected health. As reported by Time Magazine:23

“What they found was that the added sugars were significantly more harmful. Fructose was linked to worsening insulin levels and worsening glucose tolerance, which is a driver for prediabetes. It caused harmful fat storage — visceral fat on the abdomen — and promoted several markers for poor health like inflammation and high blood pressure.

‘We clearly showed that sugar is the principal driver of diabetes,’ says lead study author James J. DiNicolantonio, a cardiovascular research scientist at Saint Luke’s Mid America Heart Institute. ‘A sugar calorie is much more harmful.'”

Another more recent study published in 201724 found fructose promotes complications in glucose metabolism and alters lipid profiles associated with an inflammatory response. The researchers found this implied a systemic picture of insulin resistance.

Choline Deficiency Also Plays a Key Role in Fatty Liver Disease

Choline is a compound in living tissue and is important in the synthesis and transportation of lipids (fats). It was discovered in 186225 and officially recognized as an essential nutrient in 1998.26

Several studies27,28 have linked higher intake of choline to a range of benefits and, in fact, it appears to be a key factor in preventing the development of fatty liver disease. By enhancing secretion of very low density lipoproteins (VLDL)29 in your liver, required to safely transport fat out, choline may protect your liver health.

Epigenetic mechanisms30 of choline also explain how it helps maintain healthy liver function. Dietary choline is an important modifier of DNA and modulates expression of many of the pathways involved in liver function.

Chris Masterjohn, who has a Ph.D. in nutritional sciences,31 proposes choline deficiency is a significant trigger of NAFLD and believes the rise in NAFLD is largely the result of rejecting liver and egg yolks in the diet:

“More specifically, I currently believe that dietary fat, whether saturated or unsaturated, and anything that the liver likes to turn into fat, like fructose and ethanol, will promote the accumulation of fat as long as we don’t get enough choline.”

In a 2010 article,32 Masterjohn reviews the medical literature supporting this view. The link between choline and fatty liver initially emerged from research into Type 1 diabetes. Studies in the 1930s demonstrated lecithin found egg yolk (containing high amounts of choline) could cure fatty liver disease in Type 1 diabetic dogs. They later found choline alone provided the same benefit.

More Ways to Support Your Liver Health

Hints to additional ways of supporting your liver health may be found in the commonly identified risk factors for NAFLD. In addition to reducing or eliminating processed fructose from your diet and including foods with choline, other modifiable factors that can have a significant impact on the development of NAFLD include:33,34

  • Maintaining a healthy weight — Managing a healthy weight requires more than monitoring your calorie intake and energy expenditure. For a full explanation of one of the master keys to healthy eating, see “My Updated Nutrition Plan — Your Guide to Optimal Health.”
  • Exercising regularly — Regular movement and exercise benefits your body by improving insulin sensitivity, supporting your metabolism and mitochondrial health, helping to manage weight and blood pressure, toning muscle and improving your balance. Exercise also improves your sleep quality, mood and mental health. There is a long list of benefits — including reducing your risk of NAFLD.
  • Limiting medications — Limit any medications to those necessary and follow dosing recommendations. Some medications increase your risk of NAFLD and other health conditions. Reduce those risks by making lifestyle changes to minimize your dependence on medications.
  • Managing high blood pressure — High blood pressure increases your risk of cardiovascular disease, dementia and NAFLD. There are several natural methods of reducing high blood pressure while working with your physician to wean off medication.
  • Reducing insulin resistance — Insulin resistance may lead to metabolic syndrome, prediabetes and Type 2 diabetes, all precursors to NAFLD. For an overview of insulin resistance and how to reduce your risk of metabolic disease, see my previous article, “Research Proves Causation — Sugar Consumption Increases Risk for Chronic Disease.”

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