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Month: September 2019

A Skeptical Review of the Evidence for Metformin

A Skeptical Review of the Evidence for Metformin

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This review paper more or less leans towards my thoughts on metformin as a treatment to slow aging: the animal data is not great, the human data is a single study, the effect size on life span is far too small to care about, and the detrimental side effects are large in comparison to that effect size. The strategy of upregulating stress response mechanisms via drugs such as metformin is a poor strategy for long-lived species, as we clearly don’t exhibit the sizable gains in life span that occur in short lived species such as mice under these circumstances. Metformin, in turn, is a low performance example of this strategy, much worse than, say, the practice of calorie restriction or mTOR inhibitors.


Metformin is sometimes proposed to be an “anti-aging” drug, based on preclinical experiments with lower-order organisms and numerous retrospective data on beneficial health outcomes for type 2 diabetics. Large prospective, placebo-controlled trials are planned, in pilot stage, or running, to find a new use (or indication) for an aging population. In 2015, Nir Barzilai met with regulators from the FDA to discuss the now famous phase III multi-site TAME (Targeting Aging with Metformin) trial. The acronym chosen and the intention behind it – namely, that aging is a “disorder” that can be treated like any other disease – was a clear provocation. The FDA’s mandate is to regulate medications and devices to cure diseases or aid in their diagnosis, but aging is not (yet) an indication. Interestingly, frailty is missing from the proposed composite outcome. Other ongoing trials (e.g., NCT02570672) with metformin provide arguments that frailty may be an important endpoint. It will be interesting to compare the results with the ongoing fisetin trial (NCT03675724).

Although widely cited as evidence for the small effects of 0.1% metformin in the diet on the lifespan of older male inbred mice, earlier results obtained by researchers should be dismissed: the National Institute on Aging Interventions Testing Program could not replicate the findings regarding an extension of the lifespan with 0.1% metformin. The negative results were obtained at three different locations using genetically heterogeneous female and male mice.

The rationale for the ongoing or planned metformin trials is almost exclusively based on observations (associations) of potential benefits in a diabetic (or prediabetic) population. Its efficacy even in an at-risk cohort of aged people has not yet been proven. Metformin is associated with a higher risk of vitamin B12 and vitamin B6 deficiency, which may result in an increased risk of cognitive dysfunction. Supplementation is strongly recommended to metformin users.

Of greater concern are the results of small trials in which the effects of metformin on metabolic responses to exercise or on cardiorespiratory fitness were tested. In a placebo-controlled, double-blind, crossover trial with healthy young subjects, metformin caused a small but significant decline in maximal aerobic capacity. A double-blind, placebo-controlled landmark trial with older adults with one risk factor for type 2 diabetes investigated the effects of metformin and 12 weeks of aerobic exercise. Contrary to expectations – namely, that the effects of exercise and the drug would be additive – “metformin attenuated the increase in whole-body insulin sensitivity and abrogated the exercise-mediated increase in skeletal muscle mitochondrial respiration.”

Link: https://doi.org/10.1159/000502257

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A Non-Invasive Approach to Measuring Cellular Senescence in the Kidney

A Non-Invasive Approach to Measuring Cellular Senescence in the Kidney

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Researchers here provide evidence that the presence in the urine of extracellular vesicles carrying p16 as a part of their cargo might be used as a way to assess cellular senescence levels in the kidney. The presence of lingering senescent cells increases with age, and these cells cause chronic inflammation and tissue dysfunction in proportion to their numbers. With rapid growth in the clinical development of senolytic drugs capable of clearing senescent cells from aged tissues, and the present availability of a few proven and potential senolytic treatments such as the dasatinib and quercetin combination, there is a strong need for ways to quantify the burden of senescent cells in humans. Simple, low-cost tests that can run before and after a senolytic treatment would go a long way towards quantifying the degree to which the presently available approaches actually work.


Hypertension may be associated with renal cellular injury. Cells in distress release extracellular vesicles (EVs), and their numbers in urine may reflect renal injury. Cellular senescence, an irreversible growth arrest in response to a noxious milieu, is characterized by release of proinflammatory cytokines. We hypothesized that EVs released by senescent nephron cells can be identified in urine of patients with hypertension.

We recruited patients with essential hypertension (EH) or renovascular hypertension and healthy volunteers. Renal oxygenation was assessed using magnetic resonance imaging and blood samples collected from both renal veins for cytokine-level measurements. EVs isolated from urine samples were characterized by imaging flow cytometry based on specific markers, including p16 (senescence marker), calyxin (podocytes), urate transporter 1 (proximal tubules), uromodulin (ascending limb of Henle’s loop), and prominin-2 (distal tubules).

Overall percentage of urinary p16+ EVs was elevated in EH and renovascular hypertension patients compared with healthy volunteers and correlated inversely with renal function and directly with renal vein cytokine levels. Urinary levels of p16+/urate transporter 1+ were elevated in all hypertensive subjects compared with healthy volunteers, whereas p16+/prominin-2+ levels were elevated only in EH versus healthy volunteers and p16+/uromodulin+ in renovascular hypertension versus EH.

In conclusion, levels of p16+ EVs are elevated in urine of hypertensive patients and may reflect increased proximal tubular cellular senescence. In EH, EVs originate also from distal tubules and in renovascular hypertension from Henle’s loop. Hence, urinary EVs levels may be useful to identify intrarenal sites of cellular senescence.

Link: https://doi.org/10.1161/JAHA.119.012584

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Senescent Cells Implicated in Age-Related Changes in Blood Clotting

Senescent Cells Implicated in Age-Related Changes in Blood Clotting

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Senescent cells are created constantly in the body as the result of a number of processes: the Hayflick limit, wound healing, a toxic local environment, DNA damage, and so forth. Near all are destroyed quite quickly, either via programmed cell death or by the immune system. Some few linger, however, and secrete a potent mix of molecules known as the senescence-associated secretory phenotype (SASP). The SASP produces wide-ranging damage and dysfunction in tissues, causing issues such as chronic inflammation, fibrosis, and harmful behavior or increased senescence in nearby cells. Thus senescent cell burden is one of the important causes of aging, and efforts to produce senolytic therapies capable of selectively destroying these cells are a very important new branch of medicine.

As noted in today’s scientific materials, researchers have recently provided data to associate the burden of senescent cells in older individuals with detrimental changes in blood clotting. This adds one more item to a very long list of harmful effects resulting the SASP. With age, blood clots form more readily, and in inappropriate circumstances, such as inside major blood vessels. This can cause serious issues such as thrombosis, the blocking of blood vessels and consequent ischemia, or worse, such as a stroke or heart attack should a sizable clot fragment and the fragments block a more vital blood vessel elsewhere.

The data here associating components of the SASP with increased susceptibility to blood clotting is interesting to compare with a recent review paper on changes in platelet function with age. The biochemistry of the age-related hyperactivity of platelets, leading to increased clotting, has been examined in a proximate sense, but reaching backwards to root causes is something that the research community has never been all that good at following through on. The work here is a good example of starting with a known cause of aging and working forwards, a much more efficient approach, and one that must become more widespread in the research community if we are to see meaningful progress in treatments for age-related conditions in the years ahead.

Cellular senescence is associated with age-related blood clots


Cells that become senescent irrevocably stop dividing under stress, spewing out a mix of inflammatory proteins that lead to chronic inflammation as more and more of the cells accumulate over time. Researchers have identified 44 specific senescence-associated proteins that are involved in blood clotting, marking the first time that cellular senescence has been associated with age-related blood clots. “The incidence of venous thrombosis, which includes deep vein thrombosis and pulmonary embolism is extremely low until the age of 45, when it begins to rise rapidly. Over time it becomes a major risk factor for death. By 80, the condition affects five to six people per thousand individuals. Blood clots are also a serious side effect of chemotherapy, which sets off a cascade of senescence in those undergoing treatment. That’s why blood thinners, which carry their own risks, are often included in treatment protocols.”

In this study, researchers validated the expression of some of the specific factors in cultured cells and in mice, which were treated with doxorubicin, a widely-used chemotherapy drug which induces widespread senescence. Those mice showed increased blood clotting, similar to what happens in humans who undergo chemotherapy. “Conversely, when we selectively removed senescent cells in specially bred transgenic mice, the increased clotting caused by doxorubicin went away.”

SILAC Analysis Reveals Increased Secretion of Hemostasis-Related Factors by Senescent Cells


Cellular senescence irreversibly arrests cell proliferation, accompanied by a multi-component senescence-associated secretory phenotype (SASP) that participates in several age-related diseases. Using stable isotope labeling with amino acids (SILACs) and cultured cells, we identify 343 SASP proteins that senescent human fibroblasts secrete at 2-fold or higher levels compared with quiescent cell counterparts. Bioinformatic analysis reveals that 44 of these proteins participate in hemostasis, a process not previously linked with cellular senescence.

We validated the expression of some of these SASP factors in cultured cells and in vivo. Mice treated with the chemotherapeutic agent doxorubicin, which induces widespread cellular senescence in vivo, show increased blood clotting. Conversely, selective removal of senescent cells using transgenic p16-3MR mice showed that clearing senescent cells attenuates the increased clotting caused by doxorubicin. Our study provides an in-depth, unbiased analysis of the SASP and unveils a function for cellular senescence in hemostasis.

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16 Health Benefits of Dandelion

16 Health Benefits of Dandelion

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Dandelion is well-known as a sturdy, prolific weed that often grows unwanted in gardens, lawns, fields and playgrounds, but it’s actually an herb that has many benefits. From the dandelion leaves and roots to its stems and flowers, every part of this plant is useful. Read on to find out more about the benefits of dandelion herb and the ways you can use it to your health’s advantage.

What Is Dandelion?

Dandelion (Taraxacum officinale) is an herbaceous perennial that belongs to the Asteraceae family of plants,1 along with daises and sunflowers.2 Native to Europe, dandelion seeds were brought by American colonists to America, where they were initially planted for culinary and therapeutic use. They have since spread far and wide.3

There are many plants that look similar to dandelion, such as cat’s ear and false dandelion. If you’re planning to use this herb, it’s important to be able to tell it apart from its lookalikes. Known for its bright yellow blossoms, dandelion also has smooth, deeply toothed leaves and hollow stems that neither branch out nor produce multiple flowers.4

According to The Spruce Eats, the teeth of dandelion leaves “point back toward the center of the basal rosette,” unlike its plant lookalikes whose teeth “point forward, out and away from the center of the plant.”5 Its leaves also protect it against being pulled out, making it harder for you to extract dandelions when they grow in areas where you don’t want them.6

Dandelion is a resilient plant that can grow in any kind of soil, regardless of drainage or exposure to sunlight. To keep it from sowing itself and taking over your garden, it’s recommended that you harvest it regularly.7

Dandelion Root’s Benefits and Uses

Dandelion has a dark brown, fleshy and brittle taproot that is 2 to 3 centimeters (approximately 1 inch) wide and at least 15 centimeters (6 inches) long. Although dandelion root is available all year-round, it’s best to harvest it before it seeds, preferably during early spring or late fall, since this is when it has higher amounts of nutrients.8

According to the Journal of the Society for Biomedical Diabetes Research, dandelion root contains carotenoids, minerals, vitamins and various bioactive components, including sesquiterpene lactones, chlorogenic acid (CGA) and chicoric acid (CRA), to name a few.9 These compounds contribute to dandelion root’s medicinal properties, which include:10,11,12

  • Anti-rheumatic
  • Anti-hyperglycemic
  • Hepatoprotective
  • Anticancer

Dandelion root can be roasted, ground and used as a coffee substitute. When used as a vegetable, it has a mild flavor that some may find uninteresting.13 Dried dandelion root is also used to make dandelion root tea.14

Dandelion Uses for Your Home and Health

Different parts of the dandelion plant can be used as:

1. Food ingredients — Besides consuming dandelion root as a vegetable or using it to make coffee and tea, you can use the leaves of this plant like any leafy green. Dandelion greens have a fresh and slightly bitter flavor, making them a good substitute for spinach. However, their taste can become overpowering as the weather becomes warmer. If they’re too bitter for your taste, you can blanch the leaves to make them more palatable.

Unopened dandelion flowers can also be pickled, boiled or eaten raw in salads. Open flowers, on the other hand, can be used to make wine, jelly, cookies and bread. Be sure to remove the calyces at their base before adding the flowers to your food, as they taste bitter.15

2. Infused oils — You can make infused dandelion oil from the plant’s flowers and use it topically to help relieve muscle pain. You can also use it to make a salve or balm, which can be scented by blending it with other essential oils like lavender.16

3. Ornamental plants — While many gardeners would eradicate dandelions before they spread, this ornamental plant can be a good addition to your flower or herb garden if you want a splash of cheerful, bright yellow color. Just be sure to harvest it regularly to keep it under control.17

You’ll also play a part in protecting nature by letting some dandelions grow in your garden. According to The Guardian, dandelions are an “easily available source of food” for pollinators, including bees, hoverflies, butterflies, beetles and even birds.18

4. Fertilizer — If you harvested more dandelions than you can use, don’t throw the excess out just yet. Instead, use them as an herbal fertilizer. They contain micronutrients that can enrich your garden’s soil.19

16 Dandelion Benefits You Should Know About

Dandelion has a long history of medicinal use, particularly in Traditional Chinese Medicine (TCM) as well as traditional Arabic, Indian and Russian medical systems.20,21 This herb may be beneficial for your well-being by helping to:

1. Fight free radicals Studies have shown that dandelion extract contains phenolic components that may help inhibit oxidative damage.22,23,24

2. Reduce the risk for cancer — According to a study published in the journal Oncotarget, aqueous dandelion root extract may be a safe and effective alternative to chemotherapies, as it “efficiently and selectively triggers programmed cell death pathways.”25

3. Lower cholesterol levels — An animal study published in the International Journal of Molecular Sciences evaluated the potential hypolipidemic properties of dandelion root and leaf extract. Researchers found that it may help improve levels of high-density lipoprotein (good cholesterol) while reducing serum total cholesterol, triglycerides and low-density lipoprotein (bad cholesterol).26

4. Reduce the risk for Type 2 diabetes According to a study published in the Journal of the Society for Biomedical Diabetes Research, the bioactive components in dandelion, which includes sesquiterpene lactones, taraxasterol (TS), taraxerol, CGA and CRA, may have potential antidiabetic actions.27

5. Inhibit inflammation The sesquiterpene lactones and other phenolic substances present in dandelion have been found to contribute to its anti-inflammatory properties.28 By fighting inflammation, dandelion may help reduce the risk for inflammation-related diseases such as heart disease, arthritis, diabetes and Alzheimer’s.29

6. Regulate blood pressure levels — Dandelion may help lower blood pressure levels and reduce the risk for cardiovascular diseases with its hypolipidemic property.30 It’s also a good source of potassium,31 which may help normalize blood pressure levels by regulating the effects of sodium and easing the tension of the blood vessel walls.32

7. Maintain healthy weight — According to a study published in the Journal for Nurse Practitioners, bitter herbs like dandelion root may be taken as a liquid or tea before eating to help “stimulate gastric secretions and promote fat and cholesterol breakdown.”33

8. Improve digestion — An animal study in the journal Neurogastroenterology and Motility found that dandelion contains compounds that may help decrease the resistance of food moving from the stomach to the small intestine, ultimately accelerating the gastric emptying rate.34

9. Boost immune function — Dandelion may help support optimal immune health with its antibacterial, antiviral, antifungal, antioxidant and anti-inflammatory properties.35

10. Alleviate arthritis symptoms According to an animal study published in the journal Experimental and Therapeutic Medicine, the taraxasterol component of dandelion may help reduce the symptoms of arthritis by modulating inflammatory responses.36

11. Reduce the risk for urinary tract infections (UTI) A study published in the journal Evidence-Based Complementary and Alternative Medicine suggests that dandelion extract may be a potential alternative to antibiotics for the management of UTI because of its “antibacterial activity against uropathogenic clinical bacteria.”37

12. Support healthy liver function — A study published in the journal Environmental Toxicology found that dandelion leaf extract exerts hepatoprotective properties against sodium dichromate, a pollutant that may cause acute liver damage, hepatocyte necrosis and DNA fragmentation.38

13. Promote healthy skin — Based on the study in the Oxidative Medicine and Cellular Longevity journal, dandelion leaf and flower extract may help reduce the risk for skin photoaging by protecting against UVB damage and suppressing the production of reactive oxygen species (ROS).39

14. Reduce the risk for anemia — A study published in the journal Advances in Hematology investigated dandelion’s traditional use for managing anemia by evaluating its effects on the blood cells of mice. Results show that dandelion extract may help increase levels of red blood cells and hemoglobin.40

15. Provide natural diuretic properties — According to a study published in the Journal of Alternative and Complementary Medicine, the ethanolic extract of dandelion “shows promise as a diuretic in humans.” Diuretics are used to help decrease the sodium in your body or to manage water retention.41

16. Improve bone health — Dandelion greens are an excellent source of vitamin K and calcium,42 which are nutrients that may help improve bone density, inhibit bone loss and reduce the risk for osteoporosis and bone fracture.43,44

Try Cooking These Tasty Dandelion Recipes

If you have freshly harvested dandelions from your garden, use them to create these delicious and healthy recipe ideas:

Dandelion and Fennel Salad

Serves: 4

Ingredients

For the salad:

1 bunch finely chopped dandelion greens

1/2 fennel bulb, thinly sliced

2 cups thinly sliced Napa cabbage

1/2 cup bean sprouts

For the dressing:

1 lemon, juiced

2 tablespoons olive oil

1/8 teaspoon sesame oil

1/4 teaspoon maple syrup

1 teaspoon tamari soy sauce

1 tablespoon mirin (found in the Asian aisle)

1 teaspoon apple cider vinegar

Procedure

  1. Place the salad ingredients in a large bowl.
  2. Mix all the dressing ingredients together, pour over the top, toss lightly, and enjoy!

(Recipe from “Healthy Recipes for Your Nutritional Type” by Dr. Mercola)

Dandelion Greens With Garlic

Serves: 4

Ingredients

  • 1 pound dandelion greens
  • 1/2 cup onion, finely chopped
  • 1 clove garlic, minced
  • 1 whole small dried hot chili pepper, seeds removed and crushed
  • 1/4 cup coconut oil
  • Salt and black pepper, to taste
  • Parmesan cheese for garnish

Procedure

  1. Wash the dandelion greens well in salted water, then cut into 2-inch pieces.
  2. Cook the leaves in a small amount of salted water in an uncovered saucepan until tender, about 10 minutes.
  3. Heat the coconut oil in a skillet over medium heat. Sauté the onion, garlic and chili pepper, stirring occasionally, until the onion is translucent.
  4. Drain the greens thoroughly, and then add them into the onion-garlic mixture.
  5. Season with salt and pepper to taste.
  6. Serve the dandelion greens with grated or shredded Parmesan cheese.

(Recipe adapted from The Spruce45)

Dandelion Pumpkin Seed Pesto

Ingredients

  • 3/4 cup unsalted hulled green pumpkin seeds
  • 3 garlic cloves, minced
  • 1/4 cup freshly grated Parmesan cheese
  • 1 bunch dandelion greens (about 2 cups, loosely packed)
  • 1 tablespoon lemon juice
  • 1/2 cup extra virgin olive oil
  • 1/2 teaspoon kosher salt
  • Black pepper, to taste

Procedure

  1. Heat the oven to 350 degrees Fahrenheit. Pour the pumpkin seeds onto a shallow-rimmed baking sheet and roast until just fragrant, about five minutes. Remove from the oven and allow to cool.
  2. Pulse the garlic and pumpkin seeds together in a food processor until finely chopped.
  3. Add in the Parmesan cheese, dandelion greens and lemon juice, and process continuously until combined. Stop the processor occasionally to scrape down the sides of the bowl. The pesto will be very thick and difficult to process after a while.
  4. With the blade running, slowly pour in the olive oil and process until the pesto is smooth. Season with salt and pepper, to taste.

(Recipe adapted from The Kitchn46)

Appalachian Style Fried Dandelions

Ingredients

  • 2 cups coconut flour
  • 2 tablespoons salt
  • 1 tablespoon ground black pepper
  • 4 organic, free-range eggs
  • 80 unopened dandelion blossoms, stems removed
  • 1/2 cup grass fed butter

Procedure

  1. Combine the coconut flour, salt and pepper in a mixing bowl and set aside.
  2. Beat the eggs in a mixing bowl, then add in in the dandelion blossoms. Mix well until the flowers are completely coated.
  3. Melt the butter in a large skillet over medium heat.
  4. Remove half the dandelions from the egg mixture, allowing the excess egg to drip away.
  5. Toss the flowers in seasoned coconut flour until completely coated, then toss them between your hands to remove the excess flour.
  6. Cook the flowers in melted butter until golden brown, stirring occasionally, about five minutes.
  7. Set them on a paper towel-lined plate to drain the excess butter. Repeat with the remaining dandelion flowers.

(Recipe adapted from All Recipes47)

Take a Sip of Dandelion Tea

Dandelion tea is an herbal infusion often made from the dandelion leaves and roots.48 If you want a milder flavor, you should use its blossoms instead.49 The part of the plant used to make tea affects the health benefits it bestows. For instance, dandelion leaf tea has diuretic and anti-inflammatory affects, whereas dandelion root tea may help aid digestion and immune function.50

If you want to know how to make dandelion tea and discover more about the benefits it offers, check out the article, “9 Health Benefits of Dandelion Tea.”

Dandelion Supplements Are Also Available

While dandelion leaves and roots are often consumed cooked or raw, they also can be used to make an herbal supplement in capsule and extract form. According to the National Center of Complementary and Integrative Health, “dandelion as a dietary supplement is used as a blood ‘tonic,’ as a diuretic, for minor digestive problems, and for other purposes.”51

Use Dandelions That Come From a Reputable Source

Although dandelions offer a number of potential health benefits, not all of them are safe to consume. Dandelions found in backyards, lawns and other open areas may be contaminated with herbicides, pesticides and other pollutants, so it’s best to steer clear of them unless you know for certain that they haven’t been exposed to any contaminants.52

If possible, you can buy dandelions from the local farmers market instead to make sure they’re safe to consume or, better yet, grow your own organic dandelions at home.

Frequently Asked Questions (FAQs) About Dandelions

Q: How do you get rid of dandelions?

A: The most common method for eradicating dandelions is by using herbicides, but this isn’t recommended, as these chemicals can be harmful not only for you but also for the environment.53 You can eradicate dandelions from your garden without using harmful chemicals by pulling them out by hand. Follow these steps:54

1. Water the soil to make the plant easier to pull out.

2. Using a garden spade or a pitchfork, make an incision around the taproot, wiggling the tool to loosen the soil.

3. Grip the leaves of the plant then pull it out gently. Continue tugging on the leaves until the plant breaks free. If the taproot breaks, be sure to remove the part left in the soil, as it can regenerate into a size larger than the one you’re trying to remove.55

Q: Can you eat dandelions?

A: Yes, you can eat every part of the dandelion, from its roots to its blossoms.56

Q: Are dandelions poisonous to dogs?

A: Dandelions are not poisonous to dogs.57 To find out which plants are harmful for pets, check out the article, “Just Sniffing This Poisonous Plant Could Be Deadly to Your Pet.”

Q: What are the side effects of dandelion?

A: Dandelions can cause allergic reactions in people who are sensitive to ragweed and other related plants, including daisies, chrysanthemums and marigolds.58

Q: Are dandelion flowers poisonous?

A: Dandelion flowers are not poisonous. In fact, they are edible and can be used in salads and for making wine, jellies, cookies and bread.59


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The Boost to the Unfolded Protein Response Achieved via Exercise Declines with Age

The Boost to the Unfolded Protein Response Achieved via Exercise Declines with Age

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Exercise achieves benefits to health in large part through upregulation of cellular maintenance processes. In this way it is similar to the practice of calorie restriction, but the outcome is of a lesser degree – exercise does not extend life span in laboratory species, while calorie restriction does. Nonetheless, exercise is certainly beneficial. One of the cellular maintenance processes involved is the unfolded protein response, which, as the name might suggest, clears out proteins that are improperly folded, or have otherwise become stuck at the folding stage of protein manufacture, in the endoplasmic reticulum structure of the cell. Like other maintenance processes, the unfolded protein response becomes less effective with age, for reasons that are far from fully explored. Here, researchers demonstrate this diminished effectiveness in the context of the response to exercise.


Aging is associated with the loss of skeletal muscle mass, quality, and function; decrements that have a negative influence on health span. Resistance exercise improves muscle mass and function, but there is emerging evidence that the molecular and cellular responses to anabolic stimuli (e.g., exercise and nutrition) are attenuated in older adults; a phenomenon termed anabolic resistance. The unfolded protein response (UPR) has emerged as a key regulatory pathway in skeletal muscle protein quality control and adaptations to exercise. Early evidence points to altered UPR as an explanation for age and disease related changes in protein folding and accumulation and aggregation of proteins within the endoplasmic reticulum (ER).

The influence of age on skeletal muscle adaptive UPR in response to exercise, and the relationship to other key exercise-responsive regulatory pathways is not well-understood. We evaluated age-related changes in transcriptional markers of UPR activation following a single bout of resistance exercise in 12 young (27 ± 5yrs) and 12 older (75 ± 5yrs) healthy men and women. At baseline, there were modest differences in expression of UPR-related genes in young and older adults. Following exercise, transcriptional markers of UPR pathway activation were attenuated in older adults compared to young based on specific salient UPR-related genes and gene set enrichment analysis. The coordination of post-exercise transcriptional patterns between the UPR pathway, p53/p21 axis of autophagy, and satellite cell (SC) differentiation were less evident in older compared to young adults.

In conclusion, older adults exhibited decreased markers of UPR activation and reduced coordination with autophagy and SC-associated gene transcripts following a single bout of unaccustomed resistance exercise. In contrast, young adults demonstrated strong coordination between UPR genes and key regulatory gene transcripts associated with autophagy and SC differentiation in skeletal muscle post-exercise. Taken together, the present findings suggest a potential age-related impairment in the post-exercise transcriptional response supporting activation of the UPR and coordination with other exercise responsive pathways (i.e., autophagy, SC differentiation) in skeletal muscle that is likely to contribute to sarcopenia and age-related attenuation of adaptive responses to exercise.

Link: https://doi.org/10.18632/aging.102273

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Altered Calcium Transport in Aging Mitochondria is Maladaptive

Altered Calcium Transport in Aging Mitochondria is Maladaptive

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Mitochondria are the power plants of the cell, responsible for packaging energy store molecules used to power cellular processes. There are hundreds of them in any given cell, the descendants of ancient symbiotic bacteria. They replicate by fission, like bacteria, and carry a remnant of their original DNA. Mitochondrial function declines with age, a problem that appears to stem from an imbalance in mitochondrial fission that in turn impairs the ability of the cell to clear out worn and malfunctioning mitochondria via the process of autophagy. Exactly why this imbalance arises is poorly understood, but it can be added to the long, long list of maladaptive processes that emerge in response to the underlying molecular damage of aging.

Researchers here focus on another maladaptive aspect of mitochondrial function in aging cells: they exhibit altered calcium transport, which may initially compensate for other shortfalls, but then ultimately further contributes to the faltering of mitochondrial function. This is very much a downstream consequence of deeper problems.


Sometimes the more a person tries to fix a seemingly minor problem, the worse things become. Cells are no different, it turns out, though attempting to compensate for what begins as a minor deficiency or dysfunction can be dire. In the case of Alzheimer’s disease, researchers now show that mitochondrial calcium transport remodeling – what appears to be an attempt by cells to compensate for flagging energy production and metabolic dysfunction – while initially beneficial, ultimately becomes maladaptive, fueling declines in mitochondrial function, memory, and learning.

Altered calcium regulation and metabolic dysfunction have been suspected of contributing to neuronal dysfunction and Alzheimer’s development. Calcium transport into mitochondria plays an important part in many cellular functions and requires the involvement of multiple proteins to be carried out effectively. Among the key regulators of this process is a protein known as NCLX, which previously was discovered to mediate calcium efflux from heart cells. NCLX expression is also important in mitochondrial calcium efflux in neurons.

In a new study, researchers examined the role of mitochondrial calcium uptake by neurons in Alzheimer’s disease. To do so, the team used a mouse model of familial Alzheimer’s disease in which animals harbored three gene mutations that give rise to age-progressive pathology comparable to Alzheimer’s progression in human patients. As mice carrying the three mutations aged, the researchers observed a steady reduction in NCLX expression. This reduction was accompanied by decreases in the expression of proteins that limit mitochondrial calcium uptake, resulting in damaging calcium overload. NCLX loss was further linked to increases in the production of cell-damaging oxidants. When NCLX expression was restored, levels of harmful protein aggregates declined, neuronal mitochondrial calcium homeostasis was reestablished, and mice were rescued from cognitive decline.

“Our findings indicate that maladaptive remodeling of pathways to compensate for abnormalities in calcium regulation, which perhaps are meant to maintain energy production in cells, lead to neuronal dysfunction and Alzheimer’s pathology. Moreover, our data suggest that amyloid beta and tau pathology actually lie downstream of mitochondrial dysfunction in the progression of Alzheimer’s disease, which opens up a new therapeutic angle.”

Link: https://medicine.temple.edu/news/temple-scientists-identify-promising-new-target-combat-alzheimers-disease

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The Best Way to Test Your Cholesterol – Dr. Heidi Yanoti, Life Extension

The Best Way to Test Your Cholesterol – Dr. Heidi Yanoti, Life Extension

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The Best Way to Test Your Cholesterol - Dr. Heidi Yanoti, Life Extension
Dr. Heidi Yanoti, DC – Life Extension Senior Wellness Specialist

Cholesterol management is a vital part of promoting heart health. But if you are one of the millions of Americans struggling with high cholesterol, you have probably heard and seen conflicting information.1 Is the focus on cholesterol a myth? Or do you need to lower cholesterol to prevent heart attacks? September is Cholesterol Education Month, so it’s a great time to learn the facts!

Related (Podcast): Is Your Cholesterol on the Level? Statin Alternatives for Lowering Cholesterol

Are standard cholesterol tests enough?

When doctors first began focusing on cholesterol as a cardiovascular risk factor, their attention was on total cholesterol. We later realized that total cholesterol alone tells us little. We needed to consider its two major components, LDL (low-density lipoprotein or bad cholesterol) and HDL (high-density lipoprotein or good cholesterol), for test results to better reflect cardiovascular risk. While this was a step in the right direction, recent research shows that we need to look even more closely at cholesterol and the particles that carry it through the blood, called lipoproteins, to more fully understand cardiovascular risk.

What is the NMR Test?

NMR (nuclear magnetic resonance) spectroscopy is an advanced lipid-testing method that allows for a more in-depth assessment of the properties of lipoproteins and blood cholesterol than a conventional lipid panel.2 NMR testing goes far beyond the measurements of total cholesterol, HDL cholesterol and LDL cholesterol that standard yearly bloodwork measures. LDL particle size and LDL particle number are both important risk factors and can be used in conjunction with traditional lipid measurements to better estimate CVD (cardiovascular disease) risk.3 The NMR profile assesses LDL particle size and number.

The LDL Paradox

LDL particle number is a powerful tool for predicting heart disease.4LDL stands for low-density lipoprotein. LDL serves as a transport vehicle for cholesterol in the blood because cholesterol by itself doesn’t flow through the blood well. LDL particles can carry varying amounts of cholesterol. Studies indicate that the number of LDL particles, not just the amount of cholesterol in each LDL particle, is an important CVD risk factor.5This means that your typical yearly labs could show high amounts of LDL cholesterol, but if you are maintaining a low particle number, your heart disease risk may not necessarily be high, depending on your other CVD risk factors. The opposite can also apply: if your standard cholesterol test shows a healthy level of LDL cholesterol, you could still have an increased risk of cardiovascular disease if your LDL particle number and/or other CVD risk factors are elevated. And you may not be aware of this without running an NMR test.3

What is LDL particle size?

LDL particle number is not the only important risk factor that the NMR test can detect. LDL particle size is crucial as well. Multiple published medical studies now clearly show that the specific properties of LDL particles in your blood are important factors in your risk for heart disease.6 We now understand that if the majority of your LDL particles are large and buoyant (sometimes referred to as big and fluffy), they may pose less risk to your heart and arteries. If your LDL particles are small and dense, they can much more easily infiltrate the artery wall to cause damage and start the inflammatory process that can lead to the development of arterial plaques.6 Small LDL particles also linger in circulation longer, giving them more time to inflict damage on your arteries.6,7 One study showed that men with the smallest LDL particle size had about three-fold increased risk of ischemic heart disease than men with the largest LDL particle size.8 The NMR test not only measures the average size of your LDL particles, but also offers a count of how many of the small, dense, more-atherogenic particles are circulating.9

What about HDL?

The NMR test also gives us more details about our HDL cholesterol. It has long been known that HDL cholesterol is protective for our heart and arteries, and studies show cardiovascular and even longevity benefits for those with high amounts of HDL.10-13 You can learn even more information about HDL’s protective ability if you utilize an NMR panel. When it comes to good, protective HDL cholesterol, more particles are associated with greater protection.14 The NMR test provides a measurement of HDL particles, and the higher your HDL particle number, the more beneficial your good cholesterol is for your cardiovascular system.15

The Bottom Line

What does this really mean to the average person? If you are relying on standard lipid profiles found in basic yearly blood tests, you may not have an accurate assessment of how your cholesterol impacts your heart disease risk. The information you glean from an NMR profile will provide more robust information and serve as an invaluable tool that your physician can use to decide whether a medication is needed or choosing which nutrients may best promote your cardiovascular health.

To learn more about cholesterol management, listen to the latest episode of the Live Foreverish Podcast as Drs. Mike and Gossard discuss alternative medications and nutrients for lowering cholesterol without all of the side effects.

About the Author: Heidi Yanoti earned her Doctor of Chiropractic degree from Life University. She has been a Senior Wellness Specialist at Life Extension for over 10 years and a lifelong advocate for alternative approaches to optimal health. She enjoys sharing this passion with Life Extension customers, helping them achieve their health goals with a focus on promoting wellness. In her spare time, she enjoys reading, films and desert hikes in her Las Vegas, Nevada, home.





References:

  1. Centers for Disease Control and Prevention (CDC). High Cholesterol Facts. Accessed 9/11/2019. https://www.cdc.gov/cholesterol/facts.htm
  2. Am J Cardiol. 2002;90(8a):22i-29i.
  3. J Clin Lipidol. 2011;5(2):105-13.
  4. Curr Atheroscler Rep. 2004;6(5):381-7.
  5. J Clin Lipidol. 2007;1(6):583-92.
  6. Oxid Med Cell Longev. 2017;2017:1273042.
  7. Am J Cardiol. 2002;90(8a):30i-47i.
  8. Circulation. 1997;95(1):69-75.
  9. Circulation. 2009;119(7):931-9.
  10. J Gerontol A Biol Sci Med Sci. 2002;57(11):M712-5.
  11. Atheroscler Suppl. 2004;5(2):25-31.
  12. Age Ageing. 2007;36(5):514-20.
  13. Aging (Albany NY). 2018;10(11):3528-3540.
  14. J Am Coll Cardiol. 2012;60(6):508-16.
  15. Br J Pharmacol. 2012;167(6):1177-94.

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RAGE and Chronic Inflammation in Aging

RAGE and Chronic Inflammation in Aging

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Chronic inflammation is a very important downstream consequence of molecular damage in the progression of aging, arising from numerous causes. The past decade of work on the presence of lingering senescent cells in old tissues indicates that their signaling is significant cause. In animal studies, removing senescent cells can reverse the course of many age-related and other conditions that are primarily inflammatory in nature. Visceral fat tissue in excess amounts can accelerate the production of senescent cells, but it also generates inflammation through other mechanisms, such as debris from dead cells, signaling by non-senescent fat cells that resembles the signaling of infected cells, and so forth.

There are also numerous other contributing factors relating to the growing dysfunction of the immune system, or some of the metabolic issues that accompany excess fat tissue. The one examined in today’s open access paper is the interaction of advanced glycation end-products (AGEs) with the receptor for AGEs (RAGE). There are a couple of different issues in aging, type 2 diabetes, and obesity relating to AGEs. The more interesting one for the SENS rejuvenation research community is the accumulation of persistent cross-links in the extracellular matrix formed from glucosepane; these cross-links degrade tissue elasticity, which in turn contributes to hypertension via arterial stiffening, among many other issues. However, there are many other short-lived AGEs that arise from the diet and from cellular metabolism, and which are particularly prevalent in the distorted metabolism of obese and diabetic patients.

These short-lived AGEs produce inflammation by overactivating RAGE; this mechanism has been fairly well studied in past years, particularly in diabetic patients. As the authors of this paper note, however, even well studied parts of human biochemistry have plenty of unanswered questions left for researchers to work on. As for a number of processes that may operate to a significant degree in both diabetes and aging, it is an open question as to the degree to which RAGE is important in purely age-related dysfunction, versus other mechanisms such as the accumulation of senescent cells. Older people tend to have more fat tissue, which obscures the matter.

Is RAGE the receptor for inflammaging?


In its full-length form the receptor for advanced glycation end products, RAGE, is a multi-ligand, transmembrane receptor promoting activation of key pro-inflammatory and pro-oxidative pathways. The deleterious effects of its activation via the binding of AGEs (the advanced glycation end products after which it is named) are widely reported, especially in diabetes mellitus. Indeed, our current understanding of RAGE relies heavily upon research on this metabolic disorder, but it is simplistic to apprehend this receptor solely within a diabetic context or through its interactions with AGEs. RAGE is more broadly implicated in both immunity and inflammation: more than 28 RAGE ligands are known, many of which are damage-associated molecular patterns (DAMPs) or pathogen-associated molecular patterns (PAMPs).

RAGE can thus be more accurately considered a pattern recognition receptor (PRR), and has been labelled a “noncanonical Toll-like receptor (TLR)” by some authors. This wider involvement of RAGE signalling nevertheless remains poorly-studied relative to research involving diabetes and AGEs, but evidence is accumulating of its role in what has come to be known as “inflammaging“. RAGE deletion has been shown to be protective against both cardiovascular disease and Alzheimer’s disease in RAGE-/- mice, and while the impact of anti-RAGE therapeutics remains to be demonstrated in humans, laboratory results highlight the potential of targeting this receptor to address multiple public health issues.

RAGE has obvious similarities with other PRRs and there are acknowledged pro-aging mechanisms such as oxidative stress, mitochondrial dysfunction or inflammasome activation resulting from its interaction with several of its ligands. The concomitant, age-related increase of circulating DAMPs, and the expression of RAGE on many cell membranes, even in the absence of a pathological event, could favour low-grade, persistent, pro-inflammatory processes which in turn could drive increased production of DAMPs and expression of RAGE. This pro-aging vicious circle of events places RAGE firmly in the spotlight as a key-actor in inflammaging, not least because senescent cells also produce RAGE ligands like HMGB1 and S100s.

This hypothesis is attractive and opens up significant possibilities in the development of anti-RAGE therapeutics, but many questions remain. To what extent do the different RAGE ligands compete for binding, and how does this competition modulate its activation? Are the activated signalling pathways ligand-specific, or perhaps specific to the configuration of RAGE in its various forms? Are there negative effects to RAGE inhibition?

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Fake Meat Is Junk Food

Fake Meat Is Junk Food

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The junk food industry has a new product they are offering in exchange for your health and finances. Using strategies to position it as a healthy alternative for natural meat, the industry’s fake meat is just another name for ultraprocessed food, full of genetically engineered (GE) and pesticide-laden ingredients designed to look as much like meat as possible.

In an effort to get you hooked on it, it’s marketed as healthier and better for the environment — which may lead you to believe you’re eating good food while protecting your local air and water supplies. The manufacturers are so intent on mimicking foods found in nature that they’ve even genetically engineered “blood” for their fake meat products.1

Food critics2 are divided on the taste, with some finding the texture pleasing, but not tasting like a burger. Others say that only when the burger is piled high with caramelized onions, vegan mayo and mashed avocado, does the flavor likely approximate meat.

When it comes to organic offerings, food manufacturers would like you to believe they can improve on nature but, historically, this has been nearly impossible to achieve. Ultraprocessed foods have contributed to the obesity epidemic,3 rising rates of cardiovascular disease and an increased risk of all-cause mortality.4

If you think ultraprocessed foods are only found in the junk food aisle, though, it may surprise you to learn that, according to Current Developments in Nutrition, many foods you eat most likely include fake meat ingredients:5

“Besides salt, sugar, oils, and fats, ingredients of ultra-processed foods include food substances not commonly used in culinary preparations, such as hydrolyzed protein, modified starches, and hydrogenated or interesterified oils.

Additives whose purpose is to imitate sensorial qualities of unprocessed or minimally processed foods and their culinary preparations or to disguise undesirable qualities of the final product, such as colorants, flavorings, nonsugar sweeteners, emulsifiers, humectants, sequestrants, and firming, bulking, de-foaming, anticaking, and glazing agents.”

Health Is Not Driving a Meat Makeover

The Heart and Stroke Foundation of Canada warns you should not be swayed by deceptive marketing tactics using words such as “healthy” and “natural”6 when you make food choices. Unfortunately, it appears that some consumers believe the advertising promises.

While called a plant-based meat alternative, Beyond Burgers and Impossible Burgers are an ultraprocessed conglomeration of chemicals, concocted by pulling protein from soy and a few other processed concentrates. Amy Keating, registered dietitian and Consumer Reports nutritionist, commented:7

“… while its starting materials may be plants, the main ingredients are all highly processed concentrates, oils, and flavors. If you want the health benefits of plants, eat them as whole foods with their nutrients and fiber naturally present.”

Adding to the discussion, both Impossible Burger and Beyond Burger have nearly the same amount of total fat and calories as real beef burgers. In addition, both also have much more processed sodium added. As a reporter at NBC News so succinctly pointed out:8

“If eating more realistic fake meat was about health, the offerings would be far lower in salt content, contain fewer calories and have a bit less dietary fat. None of them do, because the point was never to live up to the marketing of healthier eating. It was to simply act as a smooth replacement for the meat we worried about eating in our day-to-day lives.”

The fake meat industry is riding the coattails of the real risk that concentrated animal feeding operations (CAFOs) pose to the environment and to human health. However, fake meat manufacturers have turned to the laboratory to boost profits and drive sales rather than support sustainable and environmentally friendly real food production.

Chemical-Packed Fake Meat Contains GE Blood

After they mimicked the look and texture of meat, manufacturers gave consumers the taste and color of blood using a compound produced by genetically engineered yeast cells.9 The compound is called soy leghemoglobin, coming from the roots of the soybean plant. On a chemical level, it’s similar to the heme iron molecule found in mammal blood and it adds some of the texture and bloody look of an all-beef patty.

But manufacturing it to scale is impossible with just soybeans —it takes one full acre of soybeans to produce 1 kilo of leghemoglobin.10 Plus, it requires genetic work in the lab to insert the soy leghemoglobin into engineered yeast cells. During the fermentation process, the GE yeast produces large quantities, in addition to dozens of other proteins.

Impossible Burger’s scientists fed the leghemoglobin to rats for 28 days to determine the risk of allergic reaction or toxicity. Dana Perls, from Friends of the Earth, pointed out that the rats exhibited alterations in blood chemistry, which the company did not follow up on.11

  Unfortunately, the U.S. Food and Drug Administration only requires research by the manufacturer to determine food safety and has not conducted any independent tests.12

Michael Hansen, Ph.D., Consumer Reports senior scientist, notes there is no long-term data demonstrating the effect of soy-like hemoglobin in humans.13 The process of manufacturing the compound yields at least another 45 by-product proteins, also consumed with the leghemoglobin.14

The FDA has classified the Impossible Burger as generally recognized as safe using data provided by the University of Nebraska and the University of Wisconsin.15 Other experts are not convinced.

According to the Center for Food Safety, 94% of the soybean crops grown in the U.S. are genetically altered.16 And, Hansen17 warns there are not enough data to determine human safety when consuming chemical compounds, as these compounds are produced from genetically altered yeast harvested from genetically altered soybeans.

Marketing Tactics Used to Convince Consumers

As I’ve written before, junk food is based on junk science, or information aimed at driving profits at the expense of your health. The fake meat industry has taken a page from other corporate interests such as the sugar and tobacco industries. You may have noticed a cycle some producers have used, beginning with hype and marketing and often ending up in a revelation, sometimes years later, that the products are not as healthy as you were told.

The cycle is lucrative and makes more money for companies than subsequent lawsuits drain. Vaping products, opioids, sugar-based products, traditional cigars and cigarettes and junk foods are just a few examples of items that haven’t lived up to the hype and marketing strategies. Meanwhile, millions — if not billions — flow into manufacturers’ pockets.

One of the claims from the fake meat industry, as an example, is that their products are sustainable and leave a smaller carbon footprint than that of traditional beef productions.

When compared to CAFO facilities, where animals are often treated inhumanely, the waste damages to air and water supplies and the administration of antibiotics that contribute to widespread antibiotic resistance, they may have something to complain about. However, moving from one broken system to another is never the answer.

Regenerative Farms Produce Clean, Healthy Environments

To help them “prove” they have a better carbon footprint than live animal farms, Impossible Burger enlisted the help of Quantis, a group of scientists and strategists who help their clients take actions based on scientific evidence.18 Beyond Meat commissioned the University of Michigan19 to conduct an assessment and compare the environmental impact of their production to that of typical beef production in the U.S.

The results were similar for both companies. According to the executive summary20 published on the Impossible Foods website, their product reduced environmental impact between 87% and 96% in the categories studied, including global warming potential, land occupation and water consumption.

In response, White Oak Pastures in Bluffton, Georgia, commissioned the same analysis by Quantis21 and published a 33-page study showing comparisons of White Oaks Pastures emissions against conventional beef production.

While the manufactured fake meat reduced its carbon footprint up to 96% in some categories, White Oaks had a net total emission in the negative numbers as compared to CAFO produced meat.22 Yes, negative. Also of note, emissions for producing beef at White Oaks Pastures was much lower than the average production of soybeans, the base for plant-based burgers and leghemoglobin.23 

Quantis also found that White Oaks Pastures beef falls within and even below the range of production of other types of protein sources, including beef, pork, chicken and soybeans. Additionally, emissions by White Oaks Pastures included a large negative soil carbon sequestration, which I’ve explained in many articles is essential to protecting against air pollution and climate change.24

Speaking to Consumer Reports, Friends of the Earth’s Perls added that the hype and advertising around alternatives to natural meat will distract from finding better solutions to environmental problems, and noted the true cost of producing fake meat cannot be known until it’s being produced on a large scale.25

These costs include damage to your health as well as to the environment. “Rather than creating new products that require more energy, more money, and more processed chemicals, why not invest in a truly sustainable system … ” Perls said.26

‘Plant-Based’ Not Enough — Others ‘Growing’ Meat in Labs

If eating plant-based, GE grown meat alternatives laced with heme molecules to mimic the presence of blood is not enough of a science fiction adventure, consider the fact that scientists in Tel Aviv are “growing” meat in the lab from stem cell cultures.27

A CBS News crew traveled to Tel Aviv to report on the story and had to sign a waiver to be able to taste the “meat.” CEO of Aleph Farms, Didier Toubia, told the crew he believes they can produce meat efficiently, more sustainably and in a healthier fashion than what has been traditionally offered.28

When the CBS reporter commented on the “delicate portion” of meat served to him, appearing in the video to be no more than a thinly-sliced, 1-inch square, the scientist cooking the “meat” said:29 “Well, just to get this portion is a lot of work.”

To get their product, the researchers have to extract stem cells from chicken and change the mix of protein. Then, they have to direct the cell growth, and it’s all a slow, involved process. Several other companies are jumping on the bandwagon, though, including Memphis Meats and Mosa Meats for beef and chicken, and Finless Foods and Wild-Type for fish.30

Memphis Meats’ leadership believes their controlled production environment may reduce the risk of bacterial contamination. But Hansen, a senior scientist at Consumer Reports,31 points out that “bacterial contamination can occur” in laboratory environments and that “antibiotics are often needed to curb bacterial growth in cultured cell products form drug companies.”

At this point, lab-produced meat is not available for sale. Kate Krueger, Ph.D., a New York-based research director focused on cellular agriculture, says it may be “four to six years before ‘ground’ meats are available and a decade or more before we see cuts like steaks,” in the grocery store.32

Choose Grass Fed, Not Genetically Altered Food

Although many see lab-created meat substitutes as the lesser of two evils when compared to the CAFO meat that’s currently dominating the market, altering the natural order of the lifecycle is not the answer. Analyses on regenerative agriculture have demonstrated holistic herd management as having a positive impact on the environment and producing healthy meat and dairy products.

Ultimately, fake food contributes to the rising number of people who suffer from health conditions related to the foods they eat, such as diabetes, heart disease and obesity. For health reasons, ecological reasons and your future, I recommend skipping meat alternatives and opting for real beef raised using regenerative farming practices.

When you do shop for meat, look for a local organic farmer or Demeter (biodynamic) and American Grassfed Association (AGA) certifications on the meat. These accreditations designate foods produced under high-quality, sustainable and environmentally sound practices.

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Risk Factors versus Lifestyle Choices in the Mortality of Old Age

Risk Factors versus Lifestyle Choices in the Mortality of Old Age

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Environmental and lifestyle choices, as numerous epidemiological studies have demonstrated, have considerable influence over health and mortality in late life. This open access paper balances lifestyle choices against a range of environmental factors and measures of the progression of aging. The authors find that a healthy lifestyle can only partially offset the effects of having a greater burden of age-related damage and its consequences, or, separately, the impact of low socioeconomic status. The former makes a great deal of sense, given the inevitability of aging as matters currently stand, with even the healthiest succumbing, while the latter is an interesting finding. It remains unclear as to the mechanisms linking socioeconomic status to aging: wealth, education, intelligence, stress, access to medical services, and other factors are closely tied and hard to pick apart in the human data.


Annual mortality among oldest-old individuals was reduced by somewhere between 0.2% and 1.3% from 1998 to 2008 in China. Impaired cognitive functions were independent predictors of all-cause mortality in very old people. Moreover, the risk of mortality is very high for the oldest-old with disabilities. Additionally, socioeconomic inequalities, obesity, cardiovascular factors, and chronic diseases are associated with mortality in the oldest-old. Conversely, healthy lifestyle practices, such as consumption of fruits and vegetables, social participation, and maintaining a normal weight, are associated with lower mortality. The question remains as to whether a healthy lifestyle and behavioral factors (e.g., never smoking and physical training) can somehow compensate for the harmful effects of the risk factors on mortality.

In this large, nationwide cohort study of Chinese oldest-old (80 years of age and older), we found that rural residence, not in marriage, lower economic level, physical disability, impaired cognitive function, and comorbidity are independent risk factors for mortality. Using these factors, we computed a weighted “risk score.” Because never smoking, never drinking, doing physical exercise, having an ideal diet, and a normal weight were independently associated with lower mortality, we also combined them to compute a weighted “protection score.” Both scores were divided into lowest, middle, and highest groups using their tertiles.

In joint effect analyses, participants with the combined highest-risk score and lowest-protection score profile had a nearly threefold higher joint death risk. These analyses show that adherence to a healthy lifestyle counteracts the negative effect of risk factors on all-cause mortality in the oldest-old by more than 20%.

Link: https://doi.org/10.18632/aging.102274

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